Advanced Liver Cancer

i'm a cancer doctor, and i walked out of my office and walked by the pharmacy in the hospital three or four years ago, and this was the cover of fortune magazine sitting in the window of the pharmacy. and so, as a cancer doctor, you look at this, and you get a little bit downhearted. but when you start to read the article by cliff, who himself is a cancer survivor, who was saved by a clinical trial

where his parents drove him from new york city to upstate new york to get an experimental therapy for -- at the time -- hodgkin's disease, which saved his life, he makes remarkable points here. and the point of the article was that we have gotten reductionist in our view of biology, in our view of cancer. for the last 50 years, we have focused on treating the individual gene

in understanding cancer, not in controlling cancer. so, this is an astounding table. and this is something that sobers us in our field everyday in that, obviously, we've made remarkable impacts on cardiovascular disease, but look at cancer. the death rate in cancer in over 50 years hasn't changed. we've made small wins in diseases like chronic myelogenous leukemia, where we have a pill that can put 100 percent of people in remission,

but in general, we haven't made an impact at all in the war on cancer. so, what i'm going to tell you today, is a little bit of why i think that's the case, and then go out of my comfort zone and tell you where i think it's going, where a new approach -- that we hope to push forward in terms of treating cancer. because this is wrong. so, what is cancer, first of all?

well, if one has a mass or an abnormal blood value, you go to a doctor, they stick a needle in. they way we make the diagnosis today is by pattern recognition: does it look normal? does it look abnormal? so, that pathologist is just like looking at this plastic bottle. this is a normal cell. this is a cancer cell. that is the state-of-the-art today in diagnosing cancer. there's no molecular test, there's no sequencing of genes that was referred to yesterday,

there's no fancy looking at the chromosomes. this is the state-of-the-art and how we do it. you know, i know very well, as a cancer doctor, i can't treat advanced cancer. so, as an aside, i firmly believe in the field of trying to identify cancer early. it is the only way you can start to fight cancer, is by catching it early. we can prevent most cancers. you know, the previous talk alluded to preventing heart disease. we could do the same in cancer. i co-founded a company called navigenics,

where, if you spit into a tube -- and we can look look at 35 or 40 genetic markers for disease, all of which are delayable in many of the cancers -- you start to identify what you could get, and then we can start to work to prevent them. because the problem is, when you have advanced cancer, we can't do that much today about it, as the statistics allude to. so, the thing about cancer is that it's a disease of the aged. why is it a disease of the aged?

because evolution doesn't care about us after we've had our children. see, evolution protected us during our childbearing years and then, after age 35 or 40 or 45, it said "it doesn't matter anymore, because they've had their progeny." so if you look at cancers, it is very rare -- extremely rare -- to have cancer in a child, on the order of thousands of cases a year. as one gets older? very, very common. why is it hard to treat? because it's heterogeneous,

and that's the perfect substrate for evolution within the cancer. it starts to select out for those bad, aggressive cells, what we call clonal selection. but, if we start to understand that cancer isn't just a molecular defect, it's something more, then we'll get to new ways of treating it, as i'll show you. so, one of the fundamental problems we have in cancer is that, right now, we describe it by a number of adjectives, symptoms: "i'm tired, i'm bloated, i have pain, etc."

you then have some anatomic descriptions, you get that ct scan: "there's a three centimeter mass in the liver." you then have some body part descriptions: "it's in the liver, in the breast, in the prostate." and that's about it. so, our dictionary for describing cancer is very, very poor. it's basically symptoms. it's manifestations of a disease. what's exciting is that over the last two or three years,

the government has spent 400 million dollars, and they've allocated another billion dollars, to what we call the cancer genome atlas project. so, it is the idea of sequencing all of the genes in the cancer, and giving us a new lexicon, a new dictionary to describe it. you know, in the mid-1850's in france, they started to describe cancer by body part. that hasn't changed in over 150 years. it is absolutely archaic that we call cancer

by prostate, by breast, by muscle. it makes no sense, if you think about it. so, obviously, the technology is here today, and, over the next several years, that will change. you will no longer go to a breast cancer clinic. you will go to a her2 amplified clinic, or an egfr activated clinic, and they will go to some of the pathogenic lesions that were involved in causing this individual cancer. so, hopefully, we will go from being the art of medicine

more to the science of medicine, and be able to do what they do in infectious disease, which is look at that organism, that bacteria, and then say, "this antibiotic makes sense, because you have a particular bacteria that will respond to it." when one is exposed to h1n1, you take tamiflu, and you can remarkably decrease the severity of symptoms and prevent many of the manifestations of the disease. why? because we know what you have, and we know how to treat it --

although we can't make vaccine in this country, but that's a different story. the cancer genome atlas is coming out now. the first cancer was done, which was brain cancer. in the next month, the end of december, you'll see ovarian cancer, and then lung cancer will come several months after. there's also a field of proteomics that i'll talk about in a few minutes, which i think is going to be the next level in terms of understanding and classifying disease. but remember, i'm not pushing genomics,

proteomics, to be a reductionist. i'm doing it so we can identify what we're up against. and there's a very important distinction there that we'll get to. in health care today, we spend most of the dollars -- in terms of treating disease -- most of the dollars in the last two years of a person's life. we spend very little, if any, dollars in terms of identifying what we're up against. if you could start to move that, to identify what you're up against, you're going to do things a hell of a lot better.

if we could even take it one step further and prevent disease, we can take it enormously the other direction, and obviously, that's where we need to go, going forward. so, this is the website of the national cancer institute. and i'm here to tell you, it's wrong. so, the website of the national cancer institute says that cancer is a genetic disease. the website says, "if you look, there's an individual mutation, and maybe a second, and maybe a third,

and that is cancer." but, as a cancer doc, this is what i see. this isn't a genetic disease. so, there you see, it's a liver with colon cancer in it, and you see into the microscope a lymph node where cancer has invaded. you see a ct scan where cancer is in the liver. cancer is an interaction of a cell that no longer is under growth control with the environment.

it's not in the abstract; it's the interaction with the environment. it's what we call a system. the goal of me as a cancer doctor is not to understand cancer. and i think that's been the fundamental problem over the last five decades, is that we have strived to understand cancer. the goal is to control cancer. and that is a very different optimization scheme, a very different strategy for all of us. i got up at the american association of cancer research,

one of the big cancer research meetings, with 20,000 people there, and i said, "we've made a mistake. we've all made a mistake, myself included, by focusing down, by being a reductionist. we need to take a step back." and, believe it or not, there were hisses in the audience. people got upset, but this is the only way we're going to go forward. you know, i was very fortunate to meet danny hillis a few years ago. we were pushed together, and neither one of us really wanted to meet the other.

i said, "do i really want to meet a guy from disney, who designed computers?" and he was saying: does he really want to meet another doctor? but people prevailed on us, and we got together, and it's been transformative in what i do, absolutely transformative. we have designed, and we have worked on the modeling -- and much of these ideas came from danny and from his team -- the modeling of cancer in the body as complex system. and i'll show you some data there where i really think it can make a difference and a new way to approach it.

the key is, when you look at these variables and you look at this data, you have to understand the data inputs. you know, if i measured your temperature over 30 days, and i asked, "what was the average temperature?" and it came back at 98.7, i would say, "great." but if during one of those days your temperature spiked to 102 for six hours, and you took tylenol and got better, etc., i would totally miss it.

so, one of the problems, the fundamental problems in medicine is that you and i, and all of us, we go to our doctor once a year. we have discrete data elements; we don't have a time function on them. earlier it was referred to this direct life device. you know, i've been using it for two and a half months. it's a staggering device, not because it tells me how many kilocalories i do every day, but because it looks, over 24 hours, what i've done in a day.

and i didn't realize that for three hours i'm sitting at my desk, and i'm not moving at all. and a lot of the functions in the data that we have as input systems here are really different than we understand them, because we're not measuring them dynamically. and so, if you think of cancer as a system, there's an input and an output and a state in the middle. so, the states, are equivalent classes of history, and the cancer patient, the input, is the environment,

the diet, the treatment, the genetic mutations. the output are our symptoms: do we have pain? is the cancer growing? do we feel bloated, etc.? most of that state is hidden. so what we do in our field is we change and input, we give aggressive chemotherapy, and we say, "did that output get better? did that pain improve, etc.?" and so, the problem is that it's not just one system, it's multiple systems on multiple scales.

it's a system of systems. and so, when you start to look at emergent systems, you can look at a neuron under a microscope. a neuron under the microscope is very elegant with little things sticking out and little things over here, but when you start to put them together in a complex system, and you start to see that it becomes a brain, and that brain can create intelligence, what we're talking about in the body,

and cancer is starting to model it like a complex system. well, the bad news is that these robust -- and robust is a key word -- emergent systems are very hard to understand in detail. the good news is you can manipulate them. you can try to control them without that fundamental understanding of every component. one of the most fundamental clinical trials in cancer came out in february in the new england journal of medicine,

where they took women who were pre-menopausal with breast cancer. so, about the worst kind of breast cancer you can get. they had gotten their chemotherapy, and then they randomized them, where half got placebo, and half got a drug called zoledronic acid that builds bone. it's used to treat osteoporosis, and they got that twice a year. they looked and, in these 1,800 women,

given twice a year a drug that builds bone, you reduce the recurrence of cancer by 35 percent. reduce occurrence of cancer by a drug that doesn't even touch the cancer. so the notion, you change the soil, the seed doesn't grow as well. you change that system, and you could have a marked effect on the cancer. nobody has ever shown -- and this will be shocking -- nobody has ever shown that most chemotherapy

actually touches a cancer cell. it's never been shown. there's all these elegant work in the tissue culture dishes, that if you give this cancer drug, you can do this effect to the cell, but the doses in those dishes are nowhere near the doses that happen in the body. if i give a woman with breast cancer a drug called taxol every three weeks, which is the standard, about 40 percent of women with metastatic cancer

have a great response to that drug. and a response is 50 percent shrinkage. well, remember that's not even an order of magnitude, but that's a different story. they then recur, i give them that same drug every week. another 30 percent will respond. they then recur, i give them that same drug over 96 hours by continuous infusion, another 20 or 30 percent will respond.

so, you can't tell me it's working by the same mechanism in all three size. it's not. we have no idea the mechanism. so the idea that chemotherapy may just be disrupting that complex system, just like building bone disrupted that system and reduced recurrence, chemotherapy may work by that same exact way. the wild thing about that trial also, was that it reduced new primaries, so new cancers, by 30 percent also. so, the problem is, yours and mine, all of our systems are changing.

they're dynamic. i mean, this is a scary slide, not to take an aside, but it looks at obesity in the world. and i'm sorry if you can't read the numbers, they're kind of small. but, if you start to look at it, that red, that dark color there, more than 75 percent of the population of those countries are obese. look a decade ago, look two decades ago: markedly different. so, our systems today are dramatically different

than our systems a decade or two ago. so the diseases we have today, which reflect patterns in the system over the last several decades, are going to change dramatically over the next decade or so based on things like this. so, this picture, although it is beautiful, is a 40-gigabyte picture of the whole proteome. so this is a drop of blood that has gone through a superconducting magnet, and we're able to get resolution

where we can start to see all of the proteins in the body. we can start to see that system. each of the red dots are where a protein has actually been identified. the power of these magnets, the power of what we can do here, is that we can see an individual neutron with this technology. so, again, this is stuff we're doing with danny hillis and a group called applied proteomics, where we can start to see individual neutron differences, and we can start to look at that system like we never have before.

so, instead of a reductionist view, we're taking a step back. so this is a woman, 46 years old, who had recurrent lung cancer. it was in her brain, in her lungs, in her liver. she had gotten carboplatin taxol, carboplatin taxotere, gemcitabine, navelbine: every drug we have she had gotten, and that disease continued to grow. she had three kids under the age of 12, and this is her ct scan.

and so what this is, is we're taking a cross-section of her body here, and you can see in the middle there is her heart, and to the side of her heart on the left there is this large tumor that will invade and will kill her, untreated, in a matter of weeks. she goes on a pill a day that targets a pathway, and again, i'm not sure if this pathway was in the system, in the cancer, but it targeted a pathway, and a month later, pow, that cancer's gone. six months later it's still gone. that cancer recurred, and she passed away three years later from lung cancer,

but she got three years from a drug whose symptoms predominately were acne. that's about it. so, the problem is that the clinical trial was done, and we were a part of it, and in the fundamental clinical trial -- the pivotal clinical trial we call the phase three, we refused to use a placebo. would you want your mother, your brother, your sister

to get a placebo if they had advanced lung cancer and had weeks to live? and the answer, obviously, is not. so, it was done on this group of patients. ten percent of people in the trial had this dramatic response that was shown here, and the drug went to the fda, and the fda said, "without a placebo, how do i know patients actually benefited from the drug?" so the morning the fda was going to meet, this was the editorial in the wall street journal.

(laughter) and so, what do you know, that drug was approved. the amazing thing is another company did the right scientific trial, where they gave half placebo and half the drug. and we learned something important there. what's interesting is they did it in south america and canada, where it's "more ethical to give placebos." they had to give it also in the u.s. to get approval, so i think there were three u.s. patients

in upstate new york who were part of the trial. but they did that, and what they found is that 70 percent of the non-responders lived much longer and did better than people who got placebo. so it challenged everything we knew in cancer, is that you don't need to get a response. you don't need to shrink the disease. if we slow the disease, we may have more of a benefit on patient survival, patient outcome, how they feel,

than if we shrink the disease. the problem is that, if i'm this doc, and i get your ct scan today and you've got a two centimeter mass in your liver, and you come back to me in three months and it's three centimeters, did that drug help you or not? how do i know? would it have been 10 centimeters, or am i giving you a drug with no benefit and significant cost? so, it's a fundamental problem.

and, again, that's where these new technologies can come in. and so, the goal obviously is that you go into your doctor's office -- well, the ultimate goal is that you prevent disease, right? the ultimate goal is that you prevent any of these things from happening. that is the most effective, cost-effective, best way we can do things today. but if one is unfortunate to get a disease, you'll go into your doctor's office, he or she will take a drop of blood, and we will start to know how to treat your disease.

the way we've approached it is the field of proteomics, again, this looking at the system. it's taking a big picture. the problem with technologies like this is that if one looks at proteins in the body, there are 11 orders of magnitude difference between the high-abundant and the low-abundant proteins. so, there's no technology in the world that can span 11 orders of magnitude. and so, a lot of what has been done with people like danny hillis and others

is to try to bring in engineering principles, try to bring the software. we can start to look at different components along this spectrum. and so, earlier was talked about cross-discipline, about collaboration. and i think one of the exciting things that is starting to happen now is that people from those fields are coming in. yesterday, the national cancer institute announced a new program called the physical sciences and oncology, where physicists, mathematicians, are brought in to think about cancer, people who never approached it before.

danny and i got 16 million dollars, they announced yesterday, to try to attach this problem. a whole new approach, instead of giving high doses of chemotherapy by different mechanisms, to try to bring technology to get a picture of what's actually happening in the body. so, just for two seconds, how these technologies work -- because i think it's important to understand it. what happens is every protein in your body is charged, so the proteins are sprayed in, the magnet spins them around,

and then there's a detector at the end. when it hit that detector is dependent on the mass and the charge. and so we can accurately -- if the magnet is big enough, and your resolution is high enough -- you can actually detect all of the proteins in the body and start to get an understanding of the individual system. and so, as a cancer doctor, instead of having paper in my chart, in your chart, and it being this thick, this is what data flow is starting to look like in our offices,

where that drop of blood is creating gigabytes of data. electronic data elements are describing every aspect of the disease. and certainly the goal is we can start to learn from every encounter and actually move forward, instead of just having encounter and encounter, without fundamental learning. so, to conclude, we need to get away from reductionist thinking. we need to start to think differently and radically. and so, i implore everyone here: think differently. come up with new ideas. tell them to me or anyone else in our field,

because over the last 59 years, nothing has changed. we need a radically different approach. you know, andy grove stepped down as chairman of the board at intel -- and andy was one of my mentors, tough individual. when andy stepped down, he said, "no technology will win. technology itself will win." and i'm a firm believer, in the field of medicine and especially cancer, that it's going to be a broad platform of technologies that will help us move forward

and hopefully help patients in the near-term. thank you very much.

Advanced Colon Cancer Symptoms

hello. it's eric bakker. author of candidacrusher. thank you for tuning into this youtube video today. today, i'd like to talk to youa bit about candida yeast infections. what is candida? what are candida yeast infections?candida is a type of fungus. it's basically a type of yeast. it is quite common for theseyeast to appear and grow inside peoples' bodies, as well as on the surface of their body. candidais commonly found in the gastrointestinal tract of people and also in the vaginal areaof women. it can also be found in the throat, mouth, and on the skin surfaces of people.it can become quite a problem when it becomes an invasive infection, and particularly inthose who have got a compromised immune system. as i mentioned, it's a normally occurringyeast that inhabits the gastrointestinal tract

of more than 90 percent of people. it's commonlykept in check by beneficial bacteria and other beneficial yeasts. it can migrate quite easilyfrom the vaginal area of women, from the rectal area into the vaginal area and cause vaginalthrush. this is quite a common occurrence with many women. the overgrowth can also affectmen, women, as well as children. this condition can underpin many different chronic illnesses.it's frequently misdiagnosed by many people in the health care profession. it's commonlymisdiagnosed as irritable bowel syndrome and even inflammatory bowel syndrome by lots ofpractitioners. one of the leading causes as you're going to see in this presentation isantibiotics. low-grade stress, in particular, chronic ongoing stress is often one of thebig causes of a yeast infection. but so are

diets that can be laden in sugar and yeasts.here, you can actually see a picture of candida, the particular form. you can see the littlebuds here that can break off and grow into new yeasts. candida is quite an amazing organismwith how it can reproduce and spread through the body, and it can evade detection by theimmune system. it's very clever how it can mutate, change, grow, and evade destructionby the immune system. what are some of the main causes of a candidayeast infection? well, these are the main 11 causes, and you can also see another youtubevideo on this particular slide here. antibiotic drugs are one of the leading causes of yeastinfection. since the advent of antibiotics, there has been a very big increase in yeastinfections in people right across the board.

antibiotics in meat are quite incredible howmuch antibiotics are used in poultry, for example. many thousands of kilograms of antibioticsare used every year in america and many countries across the world in the food chain, as wellas pharmaceutical drugs. antibiotics found in foods are big causes of yeast infectionsbecause they kill beneficial bacteria and allow yeast to thrive.underlying immune deficiencies. some people are actually born with immune weaknesses thatcan predispose them to a yeast infection. steroid drugs or other pharmaceutical drugscan undermine a person's health and be a causative factor. alcohol is a huge cause of yeast infections.men who drink beer regularly and women or men who drink wine or beer can be particularlyprone to yeast infections. particularly those

who are under stress, taking antibiotics,consume reasonable amounts of alcohol. you don't have to be a big drinker to get a yeastinfection. but maintaining regular alcohol consumption along with sweet foods, breads,candies, chocolates, these things can all predispose you to a yeast infection. candidafriendly diets are diets high in soda drinks, ice cream, bagels, donuts, packaged cereals,jelly, or jell-o; take away foods, all these sorts of diets can contribute to a candidayeast infection. stress can be a huge causative factor. stressactually can cause a depletion of the hormone "cortisol" long term, and cortisol is a veryimportant steroid hormone produced by the adrenal gland, which has a very powerful effecton creating a strong immune presence in the

body. with chronic ongoing stress, we cancommonly find a person has an increased susceptibility to a yeast infection.exposure to toxins, chemicals, heavy metals, mercury fillings has been linked with theliberation of methyl mercury in the mouth. some experts argue that there is no associationwith yeast infections, but many other experts believe there is a clear-cut association withmethyl mercury and yeast infection. diabetes. of course, people with particularlytype 2 diabetes will have elevated blood sugar levels that can make a person more prone tohaving a yeast infection. as they maintain unchecked levels of blood sugar, it makesit easy for candida to grow. and, of course, they urinate out large amounts of sugar andthat can cause all sorts of yeast problems

in that part of the body.chlorinated water has been implicated. chlorine can be anti-bacterial and allow yeast to thrive.and, of course, mold exposure. we find in new zealand and many other temperate zoneswhere people use a lot of heating inside that mold can be a big causative factor and helpto increase yeast infection in many people. what are some of the typical signs and symptomsof a yeast infection? you can read them here and you can also look at yeastinfection.org.i've got quite a few pages up on that website showing you the common signs and symptomsand the less common signs and symptoms. but these are the common ones you'll find withdigestive problems like bloating and gas, food allergies, vaginal thrush, mood disorders,poor memory, poor concentration, brain fog

is a key symptom we find quite a lot, tiredand malaise, toenail fungus, tinea, athlete's foot, urinary candida manifestations, menstrualproblems, libido issues, painful muscles and joints, constipation and diarrhea are verycommon symptoms, many sorts of respiratory allergies and issues, sinusitis, hay fever,persistent cough, phlegm, even heart arrhythmias have been linked with yeast infections. andpoor nails and skin are typical signs and symptoms. lesser common ones can be headaches,but i see them quite a bit, too, in people with chronic infections.candida can affect your body in multiple ways. here, you can see a typical concern with thefeet, athlete's foot here, very common with people. and toenails can look quite distortedand quite terrible. libido can be affected

because when a woman has vaginal thrush ora guy has jock itch, it can undermine the ability for people to be intimate in theirrelationship. skin manifestations, very, very common with yeast infections and commonlymisdiagnosed as being psoriasis or another kind of a skin condition.anxiety, depression, lots of stressed people can get this condition. lots of bloating andgas. we commonly see this with people. lots of burping. lots of farting. very common withbeer drinkers and ice cream eaters and people who crave sweets. they get a lot of fermentationdysbiosis, so poor bacteria and yeast will thrive in this whole gut area.here, we've got periorbital around the mouth kind of a rash. this could easily be misdiagnosedas being dermatitis, but a skin scraping and

culture will soon reveal that it is, indeed,a yeast infection. here, we have a gentlemen with probably a sinus headache, not feelinggood at all, maybe taking pain relief, probably not knowing that he's probably got an aspergillusor a yeast kind of infection there in the maxillary sinus or in the frontal sinus. avery common manifestation of a yeast infection is a sinus infection.here, we have a lady with a skin rash of the hand, another yeast kind of infection. here,we have a gentlemen who's coughing. it's common to have mucous, phlegm, and post-nasal dripwith a yeast infection. and, of course, stomach cramps, bowel issues, gas, constipation, diarrhea,bloating, pain in the small joints. candida can cause lots of low-grade inflammationsin the body. it can cause a lot of pain. you

can see particularly common here. they havepain on the left side lower down in the abdominal region. the descending colon, the sigmoidcolon, is a key area i find where people will often have issues. it can commonly be misdiagnosedas constipation or bowel pockets, diverticulitis, when, in fact, it can be a yeast infectioncommon in the bowel. these are some quite awful toenails that isee from time to time in people. patients sometimes use drugs like lamisil, but teatree oil will be found quite effective in this case. here, we have a typical case ofjock itch. i see jock itch in many males. here, we have a psoriatic lesion. i'm currentlyworking on an e-book on psoriasis because i see psoriasis to be mainly a yeast infection.once i clear candida up in a psoriasis patient,

the psoriasis disappears. i have verifiedthis in well over 100 cases. the common medical approach of candida infections,candida, is generally undiagnosed. a proper stool test is not really performed on thesepatients. sometimes they'll have a urinary culture or smear test for thrush, but it'sseen as a nuisance illness, as a sort of side effect from antibiotics. it's treated oftenas a local problem and it's actually seen by many doctors mainly as a female problem,not even as a men's potential issue. and as i mentioned earlier, it's often incorrectlyrecognized as irritable bowel syndrome. natural medicine or natural doctors aren'tmuch different from conventional doctors, unfortunately, when it comes to chronic candidabecause it's sometimes misdiagnosed by natural

medicine practitioners. and if it is diagnosed,it's not treated adequately. it's not given the respect that it deserves. i really believethis and you can read this in my book, candida crusher, that i talk that candida, when chronic,needs to be treated with a lot of respect. blood testing can be performed to look atvarious antibodies in the blood to determine if there is an antibody production, althoughi'm not really that keen on antibody testing with candida. i believe that the comprehensivestool test is really the gold test to do in this case, if you want to really know aboutyeast. you can actually determine it microscopically, visual analysis for a microscope, or it canbe cultured. urinary indican testing. we're looking for a urine test to discover bad bacteria.and wherever there are loads of bad bacteria,

we're generally going to find some elementof a yeast infection. treatments are not sufficiently followed through.treatments are not prolonged or strong enough. it's seen as small intestinal bowel overgrowthor allergies, leaky gut syndrome, irritable bowel syndrome, inflammatory bowel syndrome,etc. many naturopaths, chiropractors, and herbalists will diagnose candida as beinggluten intolerant or an allergy that the patient will have some sort of gluten issue. not enoughemphasis is placed on stress and lifestyle. there is a capability of curing a chronicyeast infection. i have no doubt. i've helped many people overcome this condition.conventional testing. these are the four general tests that a convention doctor will do ifhe or she does deem candida to be a problem.

a urinary cultural smear, conventional stooltest for a narrow range of pathogens, an antibody blood test, and a gut fermentation test, aparticular blood test. but a functional medicine practitioner or a naturopath will be moreinterested to do the enzyme-linked blood test to determine various antibodies of candidasuch as igm, iga, and igg. these things may not mean much to you, all these terms i'musing, but i will certainly elaborate on these terms in other more comprehensive video clips,in time, on the candida crusher youtube channel. the comprehensive stool test, i believe, isthe best way to determine, not just candida, but a whole raft of other dysfunctions inthe digestive system that many patients with candida actually present with. we can actuallydetermine by what kinds of foods are broken

down and passed out; we determine these tobe organic acids. certain sugars, for example, will break down to certain organic acids,and we can determine by the level in the urine to what degree a patient will have a yeastinfection. i find this simple test called indican to be quite a good test to determinehow good or poor the bacteria are. this can be done in-house. it takes five minutes inmy clinic and it's quite a good test in general to determine how poor the gut is functioning.why do i like stool testing? well, it's a non-invasive diagnostic test for assessingthe gut. it gives me a very comprehensive picture of a patient's gastrointestinal function.i can determine from a few stool samples what the bacteria levels are like. yeast can becultured. we can discover parasites. we can

look at various digestive markers. for example,amylase or pancreatic enzymes can be picked up. we can look at various absorption markersto see if the body actually is taking foods into the system. there are various metabolicmarkers and inflammation as well to see if there are any inflammatory responses goingon in the gut. again, i'll be talking more in-depth about the stool test on other youtubevideos. one point i would like to bring up is thecirculatory iga, which is the key immune marker in the stool test. and if we find it low,we'll often find this in conjunction with chronic yeast infections and also food allergiesand low beneficial bacteria. pharmaceutical drugs or viral infections can often causethis. we can often find it with inflammatory

bowel disease like colitis or crohn's as well.and stress and low-grade infections are commonly found. patients who have had past viral infectionswill often show low iga. iga is made in the small intestine. the bodywill make between one to two grams of this antibody per day. and one of the key rolesis to grab hold of pathogens, bugs, and things like that and to pull them out of the digestivesystem. so iga is a very important policeman for want of a better word. they look afterthe integrity of the small intestine, in particular. it's important to have good levels of iga.when it's high, we can certainly suspect inflammatory bowel disease if we find elevated inflammationmarkers such as lysozymes, but i'll discuss that in another video.how do we boost iga? well, colostrum is quite

good. prebiotics, certain types of fibers,cayenne pepper, saccharomyces boulardii, which is a beneficial yeast that you can have withcandida. don't confuse this with a candida yeast infection. reducing elevated cortisolwhen a person is stressed is very important to increase iga.so let's look at some of the drugs that are commonly used with a yeast infection. nystatin,named after new york state. this drug was discovered by two women quite a few yearsago. i believe it was in the 1950s or 60s this drug was discovered. it's a widely promoteddrug by dr. william crook in his book, "the yeast connection," as one of the best antifungals.it's not absorbed by the gastrointestinal tract, so the body will pass it out. it interfereswith the cells of candida. it helps to destroy

them. it can cause quite severe reactions.i've had many patients through skype consultations that have told me that after taking nystatin,they got very ill, indeed. i developed quite a strong reaction to nystatin when i tookit myself, so i'm not a big fan of this particular drug. it can create a quite strong side effect.and dr. crook said, "side effects are good. strong side effects mean strong kill." buti'm not really keen for patients to have very powerful die off reactions. i don't thinkit's really necessary with candida to have these heroic treatments.the common drugs used by many doctors, the "zole" drugs. fluconazole, for example, ordiflucan, is a very common drug that's used for vaginal thrush. fungizone, amphotericin,i think it's called, is a very powerful drug

that's often used intravenously. it's a verypowerful drug that can create very strong side effects. but fluconazole can make youquite sick, too. it can have liver toxifying effects. these drugs inhibit enzymes necessaryto convert something into yeast. by taking a zole drug, you're interferingwith the function or the structure of the membrane of yeast, so you're destroying yeastby inhibiting the reproduction and growth of it. it's not really recommended by me.the body can develop resistance to these drugs and also candida can change, mutate, be quitesmart, and become resistant to the "zole" drugs, which means you need to take higherdosages and stronger drugs to get the same effect.antibiotics are actually used for yeast infections

because many practitioners confuse candidawith a bacterial infection. not a good idea. in medicine, many doctors are trained withinfection, just give antibiotics and watch and wait approach. give these drugs firstand let's see what happens. but i don't really like this idea at all.antibiotics actually have a very powerful disturbing effect on the normal bacteriallevel of the large intestine, and they create the proliferation of a lot of bad bacteria.and then, of course, yeast will start thriving in the absence of good bacteria. it's nota good idea. good bacteria, bad bacteria get killed. yeast start coming up. and as i mentionedearlier, they're found widely in the food chain. my recommendation for foods is to eatclean meats. preferably, free from antibiotics.

look at this graph here. this is quite interesting.this is in 2011; 29.9 million pounds of antibiotics were sold for meat production in north america.antibiotics to treat sick people in the usa in 2011 were 7.7 million pounds. so let'ssay two pounds is a kilogram, so you're looking at about 3.5 million kilograms of antibioticsin one year in america, which is phenomenal. this will give you some idea of reasons whywe've got such a big problem with candida yeast infection in north america. we've gota high amount of high fructose corn syrup consumption. we've got lots of artificialsugars being consumed. we've got lots of alcohol being consumed. we've got lots of antibioticsbeing consumed. we've got lots of low-grade stress. so now you can understand how yeastinfections can be really rife and why 60 to

70 million americans suffer from a yeast infection.stress reduction is very important and you'll read all about this in section 5 of chapter7 of candida crusher. i've written extensively on stress. acute short-term stress appearsnot to be as aggravating as long-term, low-grade stress when it comes to gut problems. there'sa study that was done here in the american journal of gastroenterology in 2000. i won'tgo into these pathways here about interleukins, but you can read more about this in my book.i recommend the big cleanup in my book. before people go on the candida diet, i recommendthat they start with what i call the "warm turkey" approach. i slowly take them off ofjunk food and caffeine. i do that over a 14-day period. i wind them down slowly. this minimizesaggravations and the typical healing responses

people get, and it improves retention ratefor a patient. this is mainly something i would use for people who live a conventionalwasted lifestyle of buying supermarket foods, working a normal 40-hour a week job, and beingunder low-grade stress. these are the three stages to my candida crusherdiet approach. the meat, eggs, vegetables diet. the low allergy phase and the reintroductionphase. again, you can read about this in more detail in chapter 7 of candida crusher. i'vewritten over 200 pages on diet. it's one of the most comprehensive candida books you willfind regarding dietary advice. i go into many aspects of diet.the mevy diet, i recommend because it is really an anti-candida diet. it takes away the foodsource of the yeast. yeast does not like to

thrive on meats, blueberries, avocados, greenapples, yogurt, fresh vegetables, and eggs. these seem to be key foods. they're tastyfoods. it's a good diet. you're not going to starve on this diet. you shouldn't losea great amount of weight, so i recommend this approach for several weeks before we startintroducing other foods. then we look at a low allergy diet approach.most people with a chronic yeast infection will have leaky gut syndrome, which you canread more about on yeastinfection.org. many people with a yeast infection have had a backgroundof antibiotics or the oral contraceptive pill. they'll have poor levels of bacteria. they'llhave all sorts of gastrointestinal distress. it's best for them to come off the key allergyfoods. and the key food on this picture is

cow's milk.i can remember doing a lot of work testing young children, in particular, finding thatnearly 70 percent of 350 food allergy tests, i found kids to have a problem with cow'smilk. bananas came back about 14 percent. pineapples come back reasonably high. shellfish,things like prawns and crabs and lobsters will come back relatively often. oranges,peanuts and bread and gluten is not as common as you think. the finger's always pointedat wheat and gluten when, in fact, many people have bacterial and yeast problems that needclearing up before they start taking gluten out of their diet. i'm not a big fan of eliminatinggluten from people's diets to be honest. the reintroduction diet is something thatyou look at once you start feeling a lot better

and a lot of your key signs and symptoms startdisappearing. now, this may take four months. this may take six months. this may take 12months. this may take two months. you can read about why there is such a swing in durationin my book. i explain this in more detail. but the foods that you need to reintroducefirst are generally the foods that you discontinued that gave you the least aggravation. so you'renot going to really, for example, introduce cow's milk straight up. the foods you wantto have the most back in your diet are the foods you've got to introduce last. becausethey're often the key foods that will have caused you an issue in the first place. manypeople like alcohol. many people like cow's milk. they like bread with lots of yeast init. they like cakes, biscuits, coffees with

sugars in them and milk, lots of citrus, lotsof bananas, alcohol, so all these sort of items that we like to consume, you need tobe careful and introduce them last. let's look at some special foods. and youcan read about this in section 4 of chapter 7 of my book. i've got a great amount of detailabout the special foods. sauerkraut, for example, a very good food to eat here because of thelactic acid content that encourages the proliferation of lactobacillus good bacteria. oregano containsa component called carvacrol, a particularly essential oil that's a very powerful antifungal.coconut contains caprylic acid, a very good antifungal medium chain triglyceride. so onetablespoon of coconut oil per day is a very good antifungal. cloves also contain a powerfulessential oil that is antifungal, so i usually

recommend the consumption of one or two clovesper day. yogurt and kefir. these are very good foods that you can have. foods with culturesin them are simple to make. i've done video youtube clips on these you can look for aboutthe benefits of yogurt and kefir. the allium family, foods high in sulphur, good cleansingdetoxifying foods, and garlic, in particular, is very antifungal.various supplements i recommend, probiotics, very important to take for many differentreasons. probiotics are often beneficial bacteria found lacking in many people with a yeastinfection, and these levels need to be built up again. digestive enzymes are critical.i've written extensively on reasons why people need to supplement with pancreatic enzymesto help break down starches, in particular.

you'll realize that starches are a big problemwhen you read the gaps diet book, for example. starches are a big issue with candida. peopleneed to break them down, digest them and absorb them and excrete the waste properly. and whenenzymes help to break food down properly, bacteria can start feeding on the waste producedas a consequence of digestion and form a very healthy digestive tract. this can often holdthe key for recovery for many people, particularly people with bloating, flatulence, constipation,and diarrhea will benefit often from a well-placed enzyme in the diet. antifungal/antimicrobialsupplements are required by all candida patients. these are the three key products you can readmore about in my book. leaky gut syndrome. i don't think we'll gointo this too much on this video. it is a

condition that many people with candida sufferfrom. they start developing problems with the small bowel. breaches occur and imperfectlybroken down proteins, in particular, can bypass in through the intestinal wall and affectthe immune system and cause all sorts of immune responses. leaky gut syndrome is a key thingyou'll find with food allergies. once we overcome this syndrome, your ability to consume anincreasing amount of foods you will find will certainly be satisfying for you. many peoplewith so-called gluten problems have got leaky gut syndrome that needs fixing up. once themembrane of the small bowel is repaired, gluten should not really be a problem for many ofthese people. i've helped hundreds of patients back into gluten that were told they couldnever eat wheat products again.

what are some symptoms of leaky gut? well,abdominal pain. the sensations of pain on the left or right-hand side. bloating, constipation,gas is a big one. heartburn, brain fog, mood swings, nervousness, poor memory, wheezing,shortness of breath. you may recognize some of these things if you've got candida. andonce you clear this leaky gut up, you won't suffer so much from these problems anymore.here, we can actually see a picture of these tiny things called microvilli. you can actuallysee here the lymphatic system running up through each microvilli and the blood vessels runningaround it. and here, you can actually see the cells lining this area here. here's apicture again of the villi. these tiny little villi. and we've got this tiny little areaaround it called the "brush border." these

are tiny little hair-like projections withmucous that sits in there. in this area here, the circulatory iga is king. this is an areathat we want to build up is the health of these cells lining these villa. and once webuild these cells up nice, plump, and fat, they can do their job of absorbing nutrientsinside the gut and digestive area. we'll talk more about this on another video.a couple steps to healing the leaky gut. you need to give up alcohol for three months.it's realistic. if you can't stop drinking alcohol for this period of time, you needto turn this video off and go and look elsewhere for some type of a quick fix, which is probablygoing to be full of rubbish anyway. because if you can't give alcohol up with gut problems,i can't help you. i'm sorry. then my book

wasn't for somebody like you. most peoplethat are serious about getting well with candida have got no issues about entirely stoppingalcohol for a minimum of three months. you have to stop using non-steroidal anti-inflammatorydrugs. certain types of medications like aspirin, tylenol, paracetamol, ibuprofen, you've gotto get rid of these drugs. these drugs wreck gut function. don't believe me. go to dr.google and have a good look around and you'll see that what i'm saying is correct. non-steroidaldrugs destroy digestive function. a stool test for parasites, yeast, or bacteria.you can contact me if you want at eric@naturopath.co.nz or "nzed" for those people living in australiaor new zealand, so eric@naturopath.co.nzed and i can give you some more information andpricing on stool testing. this is a test i

recommend people have who've got chronic problems.anti-inflammatory diet is a key thing for people with leaky gut. no sugar. watch outfor white flour, in particular. not because i'm against gluten, it's because these foodsmay really play up with leaky gut. and to heal it, we need to get your diet tidied up.you need to watch out for lots of meat with fat in it, vegetable oils. i prefer extravirgin olive oil. fruits and vegetables and usually white meats like organic chicken orfresh fish is a good approach. and there are a few dietary supplements you can use as well.l glutamine, in particular, is a good amino acid to help heal the leaky gut. but if yousuffer from high anxiety, you probably want to avoid glutamine. because glutamine canturn into glutamate and it can cause problems

with people with high anxiety.malabsorption and maldigestion are things we've spoken about and they're common in peoplewith candida and leaky gut syndrome conditions. this is where a lot of digestive pains willcome from in bloating, gas, and constipation and diarrhea, also brain fog is quite commonin these people. these things tend to clear up once we start eradicating candida.irritable bowel syndrome is what i call a "garbage can" diagnosis. it tends to be wherewe lump people into when we don't know what the heck is wrong with them. ibs is anotherterm i see commonly in people with low-grade chronic stress and also with food allergies.and irritable bowel syndrome is a condition that will generally clear up to a remarkabledegree once we get rid of the bad bacteria

and we reduce candida to low levels.here's a picture of a patient's fingernails. you can see here with the white flecks onthe nails. many patients who think they're getting a heart attack, in fact, have heartburnand low levels of stomach acid, which we call hypochlorhydria that can be easily fixed upwith a digestive enzyme. flaky nails, dry nails, hair that lacks luster. these thingsoften respond well to digestive enzymes. you also need a good functioning stomach toconvert pancreatic enzymes from their inactive form to the active form. and remember, wementioned that pancreatic enzymes are very important to break starches down, so you don'tend up pushing partially broken starches into the small bowel to create lots of bad bacterialareas for them to grow on, so we don't produce

lots of gas and bloating and bowel issuesfurther downstream. the better things work upstream, the better things work downstreamin the gut. if you've got any questions, you can emailme at info@yeastinfection.org. again, my name is eric bakker. i've been in practice for25 years now and treated over 15,000 cases of candida yeast infection. this is my book,candida crusher. you can certainly have a good look at this book and if you're interestedin purchasing it, it's only $47 us dollars. it's taken me three years to write this book.i've been told my many practitioners who have a copy that it's one of the best books they'veseen on yeast infection. you can also do my comprehensive, online yeastinfection evaluation here by clicking on this

link and youtube. the youtube channel. we'vegot quite a few videos i've uploaded with many more to come. i hope you found this videoinformative and it's answered some of your questions about yeast infection. i do welcomeyour questions. and if you have got a chronic yeast infection,you can always consult with my through skype. i have patients now in over 30 countries.you can read a lot more information on my yeastinfection.org site. i've got some ofthe best articles on the internet regarding candida yeast infections. i've got my comprehensivebook, youtube channel, and the yeast evaluation test. i welcome you to use these resources.they're all at your disposal. thank you for your time and consideration.

Advanced Cervical Cancer Symptoms

tonight, on cancer: the emperor of all maladies... we have the opportunity to make progress at a level that we've never seen before. new treatments bring new hope. you're holding the cells in your hand that might save your life. the cost of cancer... getting cancer is one of the worst economic things that can happen to you... ...and the future of the fight.

if the cancer cell is evolving, then so are we. the conclusion of cancer: the emperor of all maladies. i sincerely believe that the time will come in my lifetime when we can control forms of cancer which are presently uncontrollable. i try not to exaggerate that we have found the right key. now, whether it will open the gate

into the secrecy of cancer, that remains to be seen. if we can harness the built-in immunological system, i think we can lick cancer. narrator: again and again during the 20th century, scientists had convinced themselves that they were on the verge of a single cure for the many diseases called cancer.

but with each breakthrough, cancer revealed new layers of complexity, and lasting cures remained tantalizingly out of reach. it's like so many dreamsthat we have where we can't quitereach something, where every timewe grab something, it flies offlike a ball in a pool because it's constantlyone step out of our reach, one step out of our reach.

that is why canceris like no other disease. narrator: the new millennium would witness more frustration, more debate among researchers. but it would also see steadily deepening understanding of the ways cancer develops, of how it can be predicted and prevented, of how the body's own defensescan be arrayed against it. so many discoveries in so many fields that researchers have come to believe

that real, durable cures are not only foreseeable but inevitable. the cycle of discovery over the last few decades has been incredible, and we're beginning to get a clue as to what the fundamental nature of the cancer cell is, and we're beginning to ask the question, "can we now use that knowledge "to launch a second attack,

"a more sophisticated attack, "through prevention to treatment through targeted treatments against cancer?" dick clark: in 10, 9, 8, 7, 6, 5, 4, 3, 2, 1. happy 2000. narrator: the 21st century began with the promise

of a new golden age of science as enormous progress was being made toward solving some ofthe most challenging problems, from the aids virus to the origins of the universe. no realm of science seemed poised to make greater strides than cancer research. the discovery that cancer was a genetic disease in the mid-1970s

had led to the first targeted drugs, which could, with pinpoint accuracy, strike at the very abnormalities that cause cancer. herceptin homed in on the effects of a single mutation active in about a quarter of all breast cancers. but it was the next new drug, gleevec, that especially caught the popular imagination. a simple pill active against a gene that causes cml,

a deadly type of leukemia, gleevec was the cure the cancer world had been waiting for. you could take people with hundreds of thousands of malignantwhite blood cells, give them this drug, and within weeks, the diseasewas disappearing.

many peoplein the cancer community were saying, "ok,cancer is going to be cured." there is some new hope todayin the battle against cancer. female newscaster: this drug opens a door to the future. could this be the beginningof a revolution in all kinds ofcancer treatment? gleevec becomes the new religion. it becomes the north star of the cancer galaxy. and everybody, and i mean everybody,

is suddenly focused on trying to replicate the gleevec model. if you look at the period between 2000 and 2005, it was truly extraordinary. we felt like we were in thisgolden age for cancer therapy. major investmentsby pharma, by biotech, and it just felt like we weregoing to be off to the races. narrator: but like so many promised revolutions

in cancer treatment before, targeted therapy would have toovercome the cancer cell's uncanny resilience. well, extremely quicklythe question became, "were thosegolden-era drugs-- "herceptin, gleevec--outliers? were they the exceptionand not the rule?" narrator: the discovery that genes caused cancer inspired a generation of scientists

who decided to devote their careers to translating this insight into useful applications for patients. one of them was a young researcher at johns hopkins university named bert vogelstein, who set out to learn more about the mutated genes that gave rise to the disease. vogelstein chose to focus on colon cancer,

a slow-moving disease that would be easy to monitor over time. our idea was very simple. you just compare the dna of a cancer cell to the dna of a normal cell from the same individual and see where and if it's different. ok, that's a normal colon. this is what it should look like. and here's a colon cancer.

if the dna is different, then that's a very compelling argument that those alterations are responsible for the disease. narrator: when vogelsteinbegan looking for mutated genes, the technology was primitive and the going was slow. vogelstein: logistically, one has to look through the literally billions of base pairs in a cancer-cell genome

to see what those differences are, and that was really the challenge back then. narrator: by the end of the 1980s, after years of arduous work, vogelstein had managed to identify, not one genetic mutation in colon cancer cells, but several. he had also figured out the exact sequence in which these abnormalities occurred.

a timelineof the cancer's evolution from one genetic mutation to the next. in the parlance of cancer researchers, he created what we call the vogelgram-- a sequence of likely events that contribute to the development of cancer, and it's not just one event. and you could begin to think about cancer as having a history.

vogelstein's work really pinned down the idea that cancer, genetically speaking, is a multi-step process. not one gene for most cancers, but multiple genes that lead to cancer. narrator: vogelstein's results posed a series of challenging questions-- just how complex would cancer turn out to be? how many mutations would be found

within the genomes of the major cancers like those of the lung, breast, and pancreas? and how long would it take to find them all? the answers would begin to emerge from the completion of one of the most ambitious scientific projects ever undertaken-- the mapping of every gene in the human body. bill clinton: today, the world is joining us to celebrate the completion of the first survey

of the entire human genome. without a doubt, this is the most important, most wondrous map ever produced by humankind. narrator: the announcement of the successful completion of the human genome project was a turning point for cancer researchers. the human genome project finally gave us a catalogof all the genes.

the zip codes were all laid out. we had a complete google mapsof the genomes. we could navigate anywhere, and then when we had that, we could go searchingsystematically for all the genesthat cause cancer. narrator: now that they had sequenced the dna of normal cells, researchers believed they could do the same for cancer cells. then, to find the mutated genes that trigger cancer,

all that would be needed would be a side-by-side comparison-- the genes of normal cells next to the genes of cancer cells. unlike the past, where you were looking gene by gene, one by one by one, you can now look at the entire spectrum. you can look at the landscape, as it were, of cancer and you compare, within the same individual,

the normal genome, not one gene, but every single gene with every single gene that's altered in cancer. narrator: though it seemed simple, this idea would spark a massive international effort, beginning in 2005, to collect, sequence, and analyze thousands of samples of the most common cancers. it was called the cancer genome atlas.

the cancer genome atlas was an incredible team science effort where this group got together and said, "we need to understand the atlas, "the landscape of all of the genetic changes "that can happen in cancer "to understand what is the possibility of what can go wrong." narrator: by the spring of 2008,

the first results from the atlas were ready. the most exciting meetingwas that first time where there were enough samples from brain tumors to be able to begin to say, "ok, what's new here?" previously,you've had only a blurry viewthrough the fog, and you could make out some of the mostdramatic features,

but now the fog's blown away. you can see the whole landscape of what's there and infer truth about howthose cancers happened. narrator: but as more and more results poured in, some of the initial excitement was replaced by anxiety. there could be no doubt that what vogelsteinhad glimpsed in colon cancer was just the beginning. the profoundly surprising thing

about the cancer genome atlas is it pointed out that cancers are much more genetically complex than, you know, 3, 4, 5, genes. there can be 10 genes that are altered, 20 genes. in one breast cancer specimen, 110 genes were altered. narrator: even more confounding, the majority of genetic abnormalities discovered

were not familiar oncogenes, but another type of gene called a tumor suppressor gene. unlike oncogenes, which tip cells into a frenzy of cell division, tumor suppressor genes, when damaged, fail to stop cells from dividing. tumor suppressor genes are, in a sense, the opposite of oncogenes. oncogenes kind of work like

an accelerator in a car. they drive the cell's growth, and the tumor suppressor genes are the brakes. and in many cases, the brakes are simply gone from the cell. we now realizethat virtually allhuman cancer cells have both defects--stuck accelerator pedals, hyperactive oncogenes, and defectivetumor suppressor genes,

defective brake linings, and together,those 2 defects conspire to makethe full panoply of abnormal behaviors that we associate withmalignant cells. narrator: in the span of a few years, as the true complexity of the cancer cell became clear, any hope that targeted therapies would win a quick victory over the disease

was dispelled. the cancer genome is exceedingly complex. each cancer type contains anywhere from 50 to 100 recurrent amplifications and deletions. so while the progress over the past 20 years has been impressive, it's also clear that we are dealing with the tip of the iceberg.

narrator: the discovery of cancer's complexity during the century's first decade seemed to push cures even further away. drug developers could now see the genetic landscape of cancer more clearly, but the picturewas one of intimidating chaos. however, there were still a few cancers that seemed to be causedby just 1 or 2 mutated genes. it was on these

that drug makersbegan to focus most intently. in 2003, scientists working for the swiss giant novartis believed they had found a likely target, a rare oncogene called alk. japanese researchers had shown that a mutation in the alk gene seemed to be the cause of a type of lung cancer that affects around 40,000 people a year worldwide.

though the market would be relatively small, novartis decided to pursue a drug targeted against this mutation. their scientists began by manipulating various compounds to try to block the effects of the gene. after 7 years of trial and error, they believed they had one that might work. do you see? yeah, it really looks like we have room here, right,

to put something that could fill the pocket better. [indistinct chatter] narrator: the drug, called ldk, works by filling a pocket in a protein inside the cancer cell, blocking a stream of growth signals produced by the mutated gene. it's like jamming a lock with a broken key. it's a beautiful compound.

it's actually beautifulwhen you see it fit into the pocket. it's really designedto do what it's doing, the job it's doing. man: everybody thinkstheir baby is beautiful. [laughter] the medicinal chemists have a very tough challenge. not only do they have to find a molecule that fits that pocket perfectly, they also have to simultaneously

be making sure that the changes they make in the molecule don't cause it to bind to something else and cause toxicity. and so the best analogy i can think of is it's like a rubik's cube. you can solve one side of the rubik's cube, and it's all blue and it fits into the enzyme perfectly, but you've messed up all kinds of other things,

and maybe it binds to something else that causes toxicity. chemists need to beeternal optimists 'cause 99.9%of what you do fails, and after years of workof hundreds of scientists, it all came down to one powderright here in the vial. so i take 4 of these every day, and this is what's keeping me alive, literally. narrator: in 2013, dr. juanmanuel gomez, himself a physician,

became one of the first patients ever to take ldk. woman: juanmanuel g. oh, they are calling for me. hi. this way? yeah. we're gonnatake a left. narrator: gomez had been toldthat his prognosis was dire. his lung cancer was inoperable, and chemotherapy was no longer an option. with nothing else to try,

his doctors urged him to join an early trial of the ldk drug. your shoes and step right upon the scale. all right. it was very clear to me if i didn't do anything different, i-i was not going to be here. i mean, and i was dying. i was. i mean, i-i-i-i knew. i-i-i-i could feel it.

narrator: the drug had an immediate impact. within weeks, dr. gomez's tumors began to shrink, and he was able to resume a normal life. the advent of these targeted therapies really has been miraculous for some of our patients. can you unbutton that top button for me? the disease melts away. something that chemotherapy could really never do. couple deep breaths.

when i'm saying amazing response, i'm talking about these images full of cancer with blotches pretty much throughout the lungs, and these patients would be treated with this drug, and all these patches would now just disappear. even more, i think, stunning, for us as oncologists is that patients would feel better very, very quickly. well, your labs look perfecttoday, so that's great. and your scanslook great, too.

so i looked at the chestand the abdomen and the brain. they look beautiful. no, i think you're doing great, side effects-wise. narrator: but even with drugs like ldk that show early promise in clinical trials, there is a problem-- most soon stop working. the reason why comes down to a concept familiar from infectious diseases-- resistance.

even if a drug can shut down the one key mutation in a cancer cell, the cell often mutates again and is no longer vulnerable to the effects of the drug. cancer cells are constantly mutating. in fact, the cancer itself is evolving inside your body over time so that the genetic diversity of cancer at week zero

is not the same as the genetic diversity of cancer, you know, 5 years or 10 years from now. it transforms the idea of treatment from a static idea to a dynamic idea. narrator: scientists had long understood that cancer was notthe same disease in everyone, but with the realization of cancer's mutability, they now feared it might not be the same disease in anyone. what we know todayis that each cancer

is a moving target,and very few drugs, even when they're havingfantastic clinical results, end up curing people, because the cancer becomesresistant to the drugs that we're usingin almost every case. narrator: as a doctor himself, juanmanuel gomez was aware of the possibility that his cancerwould become resistant to ldk. it is a gamble.

i mean, they don't know. you know, they probably have seen some results in some animal models, and they know the drug works. is that going to necessarily translate into a human being? no one knows. narrator: in fact, just 6 1/2 months after enrolling in the clinical trial,

gomez's cancer did become resistant to the drug, and he was forced to tryanother experimental therapy. that therapy also stopped working, and dr. gomez passed away in october 2014. gomez's experience on the ldk trial was not exceptional. when all the results were tabulated, the drug had extended the lives of all 160 patients by an average of just 7 months.

the successes of the first decade of target therapy were so enormous that when the second decade started rolling around, all of a sudden, we felt disappointed because rather than having gleevec, we were getting incremental advances. narrator: in the last decade, an average of only 4 new targeted therapies have been approved for use in patients each year,

most of whichhave extended patients' lives by just a few months. 9 of 10new experimental compounds fail. this incremental progress has come at a high price. billions of dollars in research and development. to recoup these costs, pharmaceutical companies have priced their successful cancer drugs at unprecedented levels. the reality is for the overwhelming majority

of patients and oncologists, this is one of the biggest problems in cancer care. if you look at the prices of cancer drugs before the year 2000, the average price was about maybe $5,000, $10,000 a year. and then, in the year 2012, 12 of the 13 drugs that were fda-approved

came at the price of $100,000 or more. [indistinct background chatter] narrator: at the charleston area medical center in west virginia, staff oncologist dr. suzanne cole sees the impact of the high cost of cancer care every day. hello. how are you today? i'm doing great.i didn't know you was--

yes. i'm having a baby. well, congratulations. it's not going to betoo long from now. some of our patients who are, you know, middle-class americans working normal jobs with awesome insurance, sometimes that insurance doesn't, you know, cover everything that's necessary, and there are significant medical bills

month to month to month to month. all right. so what i'm going to do is give you a standing order for labs. and i just want you to keep this in your purse. and if you're on a medication that you need to stay alive and your co-pay on that medication is $700 a month, you know, like, that's rent, that's a car payment, that's--you know,

that's a crazy amount of moneyto be forking over every month just to have access to the thing that's going to keep you alive. miss carrington,this is jennifer bass. hi there. nice to meet you. hi, jennifer. nice meeting you. she is our financial navigator, and she helps peoplein your situation get back on trackwith their insurance so that they can gettheir cancer treatment. narrator: at the charleston hospital,

a full-time employee helps patients who have no ability to pay their medical bills. appreciate it.yes, ma'am. i'm going to give youall of this you fill out once youstart getting bills. don't pay any of them.ok? ha ha ha. i can't.don't pay any of them. i'm not working now.

this is this year's patients. this is what i have worked with this year on some form of financial assistance. it is... completely full. we have ostomy supplies up here. i have mastectomy bras and mastectomy prostheses up here. this is a blood thinner.

there's a wig under my desk. ha ha. i stick things everywhere. wigs. whatever it is, i will take it. getting cancer is one of the worst economic things that can happen to you in the united states. it causes the accumulation of enormous amounts of debt, fundamentally shifts the finances of families, and what's very challenging

for a lot of patients is that it can often be a disease that ends your life. and so, sort of the resources you've accumulated that you hoped to pass on to your heirs or your surviving spouse or someone else end up being consumed in the treatment of a condition that, in some cases, is incurable.

narrator: the impact of the high cost of drugs is most acute in the united states, where drug companies set their prices. in countries where the government negotiates those prices, fewer patients choose to forego their medications rather than pay for them. in the developing world, new cancer drugsare often not even available because their cost is so high.

this is a moral issue. it's a 10% to 15% lower 5-year survival in cancer in people who are uninsured and in people who are poor and in people who are black. people should not die because they're poor. people should not die because they're uninsured. narrator: the solution to the problem of cost,

many believe, lies in understanding even more about the mechanisms of cancer so that so much money is not wasted in pursuing flawed drugs. this whole system's extremely inefficient. we are not choosing the targets appropriately or wisely, and therefore, all of these medicines are failing. so what we really need to do

is to perform more efficient research, and, really, it means to perform more efficient basic research. and that's what's going to drive down the price of cancer drugs. narrator: and yet, funding for the most promising basic research has not been so tight since the national cancer act was passed in 1971. as the directorof the national institutesof health, i live with the reality that we're not limitedby ideas,

we're limited by resources, and we're not goingas fast as we could. we are now about25% below where we were 10 years ago in terms of resourcesto do this work. we've got to figure outhow to turn that around. this is gonna be 511.53. narrator: until better and cheaper therapies are discovered, many patients and their families

are forced to make a difficult calculation. what am i willing to pay for how many months of life? you know, how do i think of that? what equation governs, you know, 3 months of life for x thousand dollars? maybe it allows somebody to see a grandson's birthday party or--or go to a wedding. those are great moments of life.

so maybe that's enough, you know. i think it's not enough for most people, and especially given the amount of effort that we've put into this--this problem. [beep] narrator: with so few new targeted therapies, treatment at most cancer hospitals around the country remains much as it has been for the last 20 years. everybody is so excited

about all of thesenew targeted therapies, but when it comes down to it, the vast majority of most of the cancers that we take care of, they are still primarilytreated with chemotherapy. there are cancer surgeons, there areradiation oncologists, but the backbone of what we dois we give chemotherapy. narrator: chemotherapy hasgotten better over the years.

by using these drugs in combination and tailoring them more effectively to each patient, doctors have made inroads against many cancers. of all patients who will be diagnosed this year, some 2/3 will survive over 5 years, and of those, many will go on to live normal lifespans. there are a lot of tumorsthat we take care ofthat are cured-- early stage breast cancer,

early stagecolon cancers, early stage prostate cancer. many of those patients will livethe whole rest of their lives and never haveany problems ever again. hey. how's it going? narrator: dr. colesees up to 25 patients a day. many will be able to live with their cancers for years or see them disappear entirely. ⶠda da da â¶

it's 8.2. yeah, i know. it's likethe best it's been. [laughter] narrator: but those she spends most time with have relapsed or been diagnosed with metastatic disease. are you better than yesterday?oh, gosh, yes. and for them, she must offera very different kind of care. i know, i knowgoing into this that the vast majorityof my patients

who come to mewith stage-4 disease are going to die. and there's nothing thati can do about that end fact because it's the natureof the disease that they have in the times that we livewith the tools that we have. any weird headaches,blurry vision? it's very hard totalk about death to somebody who's inrelatively good health, you know, somebody'swho's just been diagnosedwith a cancer.

they may not evenfeel it inside of them. and you have swollen lymph nodesall along that area, and there's onethat's kind of higher upthat i'm worried about. but if they're in a situationwhere it could happen, they need to know that that's a possibility. and i just believe in thatcore principle so deeply that it really guides me in how i talk toevery single one of my patients. tell me what you knowabout your lung cancer.

i have just really known for 3 days that i have cancer. ok. i was just diagnosed. so--so what was wrong... i remember as a resident rounding with lots offantastic physicians who would walk into a roomwith a patient. they would say,"everything is fine. "you know,you're getting better.

you'll be getting out ofthe hospital soon." and then we walk intothe hall, we walk a few steps awayfrom the door, and, you know, very casually, "oh, you know, that guy'snot long for the world." and why should we,as physicians, have all of this informationabout the patient? it's the patient's information. are you interested in knowingnumbers about your prognosis?

are you interested inthat kind of thing, or are you too overwhelmedwith all of it to-- yes, i'm the type of person that likes to know as much information as possible. when we're dealing witha stage-4 lung cancer, we know that it is nota curable situation. it is treatable, and we cando things to intervene and help you liveas long as possible, but because this cancerhas spread through the body,

it's much more likelythat this cancer is going to be the thingthat takes your life rather than something else. wow, you gave a deeper explanation than i had heard earlier today, so... it's really incredibly hard to sit down withanother human being and look them in the eyeand say, "i'm sorry,but there's nothing morethat medical science can do

to make you live longeror better." i wish that we hadsome magic medication that would make thisall disappear. all of the treatmentsare to give you as much time as possible. smith: most canceris very predictable. once it comes back,unless it's a curable disease, of which there's a-- there are a number, it's going to bethe end of that person,

and there are certain tasks that the person should dobefore they die. and that's just being, you know,as straight about it-- which i appreciate. so that you-you havea good sense of what you'rereally dealing with, and you can makethe best choices in the context of your life, knowing that we might beon limited time.

well, this just really sucks. it does. and i'm sorry. yeah, me too. smith: if you're hearing aboutthat 4 weeks before you die, you're probably not going to have a chance to go to l.a. and make up withyour brother out there. you may not have a chance to talk to your priest or rabbi at a time whenyou're really well. and all of that can be helped

by just being more honestwith people during the courseof their illness. i just had been focusing on-- all the data suggests thatdirectly addressing symptoms, relieving their pain,keeping them more functional allows them to livea longer period of time, as well asa better period of time. i've been trying to do what i want to do-- you know, live life to its fullest and to enjoy it.

well, it has a different look on it for the next couple years, i think.yes. narrator: dr. cole's approach is relatively new. for decades, so-called palliative care was almost taboo in oncology. the focus of cancer treatment was on eradicating tumors at all costs. doctors did little to alleviate the pain

or address the psychological needs of dying patients. to many doctors, the word "palliative care" was a word that they were allergic to, because it meant that telling the patient, or perhaps telling themselves more than anything else, that this was defeat. obsessed with cure, this voice of palliative care,

restoring patient autonomy, restoring patient dignity, it was pushed away into the background. narrator: the movement toward palliative care began in the 1960s in london, where a british nun named cicely saunders set up a clinic to care for patients at the end of their lives. we certainly owe a lotto cicely saunders.

she showed that one could makethe life of people who are dying much more comfortablewith adequate pain medication and with adequateemotional support. and she began to talkacross the country to nurses, oncology centers, and had a real impacton palliative care beginning in this country. narrator: today, palliative care is part of the medical training

and everyday workof more and more oncologists and oncology nurses in the united states. do you feel like, at this point, after everything that you've gone through in the last couple months and we were to have to really think about chemotherapy, you'd be wanting to do that again, or you're not sure? i'd probably reallywanting to. you'd be willing to try it?yeah. ok.

some people, they need to do everything that they can do that is possible to be done to stay on this earth. they can still say, "i love this life. i love being alive. i love being here, and i will do anything to stay." for some patients, it is a war. their experience of it is a war, and to say that it isn't is to deny them their reality. it is a war for them.

and yet, for other patients, they don't want to fight, but it's not the language of defeat. it is the language of negotiation. it is the language of what to do next given the circumstances. so, you've been in the hospital for a couple of days, and, you know, one thing thati just wanted to make sure was that you were understanding what was going onwith-with your cancer.

we've done some chemo, and it seems likeit's not really helping us slow down the cancer, and so we're going tohave to make a choice about whether you want totry to do more treatment or whether we should stop. he wants to do whatever you think is best, right? 'cause you trust her 100% with everything. and... we don't know, so we'll leave it in your hands.

ok. right now, your bodyis in a situation where we've got toget you better before we could even think aboutdoing more treatment. you know? but it's not a bad choice to...to sometimes say no to the chemotherapy and take what time thatyou have left and enjoy it and not be sickand coming back and forth.

i see the time coming. [mutters and sobs] the life you've given me already is better... will you rinse this? thanks. i just really wantwhat is best for you. i want you to feel wellfor as long as possible. you know, i want you to be free of pain,

and i don't want you to struggle at all. we're going to just focus on trying to help you get stronger so that you canget out of the hospital. ok? and once you're home,we can talk about, you know, whether it makes senseto do any more treatment or not. right. and if we decidenot to do it, then, um,i'm going to have hospicecome and be with you. ok? ok. you're doing good.you're hanging in there.

cole, voice-over:i don't know if everybody has the same opinion of what is a good death. all right, sweetie,i'll check on you tomorrow. but i think that it might be better for someone to maybe be in a place that they're comfortable, surrounded by people that they love. if you decide to pull back from treatment and go on hospice, then you have some say about how you die

and where you die and who is with you. as oncologists, we may not be curing everybody, but we are... put your arm up there. we are helping people in a very important way. all right,you good right now? yeah. healing is not always eternal life. you know, healing is sometimes helping people have a good death. there's some kind of healing in that, too.

there's an often-noted paradox that we must now honestly confront. namely, despite the extraordinary progress we've made in understanding the underlying defects in cancer cells, has to be acknowledged that we have not succeeded in controlling cancer as a human disease to the extent that i believe is possible. now, i know other...

narrator: as the first decade of the 2000s passed without the expected revolution in targeted therapy, some prominent voices in the cancer community began to call for a shift in priorities from the costly hunt for new drugs to cancer prevention. if you don't get cancer,you're not going to die from it. and that's a simple truth that we sometimes overlook

because it's intellectually not very stimulatingand exciting. persuading somebodyto quit smoking is ultimately a behavioral,a psychological exercise. has nothing to do withmolecules and genes and cells. and so people like me areessentially uninterested in it in spite of the factthat stopping people smoking will have vastly more effecton cancer mortality than anything i could hope to doin my own lifetime.

narrator: prevention-- blocking the factors that causethe disease in the first place-- had long been the forgotten front in the war on cancer. but as prevention advocates began to gain a stronger voice, they could pointto some important successes, none more so thanthe campaign to stop smoking. cigarette smoking contributessubstantially to mortality from certain specific diseases and to the overall death rate.

narrator: the anti-smoking campaign began in 1964 when the surgeon general definitively linked smoking and lung cancer. at first, the finding had little effect. the rate of smoking increased in 1964, 1965, 1966, and 1967. tell me, sir. it's been 4 years since the surgeon general's report came out

about smoking and cancer, and you're still smoking. why? because this isa long-standing habit of mine. regardless of whatthese doctors say, a lot of peoplewill not pay much attention. there's other thingsmore dangerous than smoking. narrator: it would takea much more imaginative strategy to finally begin to curb america's addiction to cigarettes. the idea was the brainchild of a 26-year-old patent attorney named john banzhaf.

it involved turning cigarette companies' reliance on television advertising against them. male announcer: marlboro, the cigarette with better makin's, brings you pro football. it was thanksgiving day. i'm sitting there with my father. we were watching all of the football games, and just over and over and over again

you see cigarette commercial, cigarette commercial, cigarette comm-- now, i'd seen hundreds, thousands, tens of thousands growing up,but just something clicked. male announcer: there's always time for a marlboro. something occurred to me, something i had learned in law school which is called the fairness doctrine, which said that if you present one side

of a quote controversial issue of public importance, you must make reasonable time available for the other side. and it occurred to me-- could that possibly apply to cigarette commercials? narrator: banzhaf wrote a letter to the federal communications commission demanding that the television networks air anti-smoking messages

alongside cigarette advertisements. to his surprise, the fcc agreed. so the american cancer society produces a set of striking anti-tobacco ads in the late 1960s, early 1970s. it's all yours. your total consumption of cigarettes so far, george. half a million. and although they're often shown by networks

late at night, they begin to have an impact on rates of smoking. [hacking cough] [mutters] [coughing continues] there were people coming up to me and saying, "i quit smoking. my father quit smoking." and then suddenly, their ads become a liability. the more they advertised,

the more people stopped smoking. they had to get off the air. narrator: in january 1971, the last smoking adappeared on american television. anti-smoking advocates would eventually persuade all 50 states to regulate cigarettes more heavily and sue tobacco companies for the healthcare costs of smoking.

paid a quarter of a trillion dollars. we killed off joe camel. we got rid of cigarette billboards. we're the model. we're the example. we did it, and we did it against these tremendous odds. narrator: from its height in the late 1960s, cigarette smokinghas declined by nearly half. as a result, lung cancer hasalso begun to trend downward. almost nothing has savedas many lives,

reduced as much suffering as our recognition of the fact that smoking causes cancer. narrator: another preventable epidemic now threatens to spread the disease. though no one is certain of the mechanism, obesity clearly conveys a higher risk of colon, breast and kidney cancers among others. it's predicted that as smoking rates

continue to slowly decline and as obesity rates continue to explode that before the end of this decade that obesity will pass tobacco use as the leading preventable cause of cancer. anti-smoking campaigns have been around for a while and have been very successful, but we still have not turned around the obesity epidemic, which, at some point we're going to have to face square on and fix.

narrator: after smoking and obesity, however, the known preventable causes of cancer have been much harder to find. radiation, sunlight, asbestos, a few viruses all have been proven to trigger the genetic mutations that give rise to cancer. still, it is estimatedthat some 40% of cancer cases have no known cause at all.

the work on what causes cancer is the most difficult form ofcancer research at the moment. we don't know the cause of most of the major killers. we really don't know what causes breast cancer, pancreas cancer, colon cancer, prostate cancer. we don't know what causes them the way we know that if you stop smoking cigarettes,

you can reduce your risk of lung cancer. narrator: many of the mutations that cause cancer are probably the result of accidental copying errors among billions of cells that divide every day. but for decades,scientists have searched for hidden triggers in the environment that might explain those cancersthat yet have no explanation. man: we live in an increasingly carcinogenic environment. this could be causing many cancer deaths.

scientists have been testing nearly every substance known to man to track down carcinogens. narrator: with so much mysterystill surrounding the disease, a series of unproven theories about what causes cancer have been paraded through the media, everything from sugar to plastics, high-tension power lines to cell phones. but proving a causal link between any agent and cancer is difficult,

and this fact has greatly increased anxiety and fear. groopman:cancer is frightening, bewildering, frustrating. many people are justendlessly trawling over trying to figure out,what did i do? where did i go? should ihave taken that vacation?was i near a nuclear reactor? you know, did i drinksome water? did i not eat organic foods? and you're saying,"look at all these scientists

"who claim to know so much, "and they can't explain to me "why me, i, this individual developed lymphomaor leukemia or breast cancer." narrator: unable to identify the causes of many cancers in the laboratory, a branch of science called epidemiology has approached the problem from the other end-- by studying the incidence of cancer in contained populations

and working backwards toward a common cause. it is very much like circumstantial evidence in a court case. an epidemiologist, much like a lawyer, is trying to figure out, often based on retrospective data, on reconstruction, what the true set of events might have been that--that caused cancer. narrator: one of the first epidemiologists

was an italian physician, bernardino ramazzini, who, in 1700, associated many diseases with occupations. goldsmithsdeveloped mercury poisoning. coal miners suffered lung disease. ramazzini's observation that childless nuns had higher rates of breast cancer laid the groundwork for understanding the role of hormones in the disease.

in the 18th century, doctors noticedthat habitual users of snuff had higher-than-normal rates of nasal cancer. in the 1950s, a concentration of rarelung cancers in shipbuilders would lead researchers to asbestos. but more often, epidemiologistshave struggled to understand the behavior of cancer.

why do some cancers appear more often in some countries than in others, even among people who recently moved there? why do cancers sometimes seemto act like infectious diseases, breaking out in small populations called clusters? cancer clusters have been particularly controversial. famous examples like those at toms river, new jersey, woburn, massachusetts,

and along love canal in upstate new york have frustrated investigators and led some to doubt that they were anything morethan a statistical mirage. cancer clusters are extremely difficult because the numbers are very small. you often go to investigate the cluster some years after it's happened, now it's gone. circumstances may have changed.

the point source of whatever it was, if there was something, may have disappeared. so it's an incredibly-- to do the detective work here is really extremely difficult. ozonoff: nobody knowshow many clusters there are and how many of themare really related to some common cause. our tools just aren'tpowerful enough, aren't good enough.

it's sort of like going into a gigantic, dark warehouse full of dangerous objects with this tiny littleminer's lamp on your head and going inand looking around and say, "gee, i don't see anything,"right? and then going out again. narrator: but even as new chemicals that cause cancer have been difficult to find, an old suspect has re-emerged-- viruses.

for a number of cancers, some very common ones, like liver cancer and cervical cancer, viruses are front and center and the major causes of those cancers. happily we have developed vaccines that can prevent infections in some of those agents, and that has reduced the incidence of cancer dramatically. tonight, we have some newswe do not get to reportoften enough in the battle against cancer.

the first large-scale testof a vaccine for cervical cancer found the drug 100% effective in blocking the virusthat causes the disease. narrator: a vaccineapproved by the fda in 2006, active against the human papillomavirus, the leading cause of cervical cancer, promises to all but eradicate the disease if children can be inoculated

before they become sexually active. when i was a resident, if youhad an abnormal pap smear, you hada total hysterectomy 'cause we didn't knowwhat else to do. you lost your fertility. and then we figured outthat it was caused by a virus, and now we have a vaccine. so my daughter'sbeen vaccinated. now, that's amazing.

that's pretty amazing. we essentially can wipe outcancer of the cervix by the hpv vaccine. narrator: the science of cancer prevention is still young and dependent on imperfect knowledge of what causes cancer. but even if it succeeded only in curtailing smoking, obesity, and the known cancer-causing viruses, it would have a profound impact on mortality.

it has been estimated that today, if society were to implement what's known about prevention, then cancer deaths could be reduced by 50%, and that's without any new research or any new discoveries. it's just implementing what is already well known. here's my cherry-flavored nulightly. looking forward to drinking this in the next several hours...

narrator: even when cancers can't be prevented, they can still be stopped if they are detected early enough. bottoms up, so to speak. heh. narrator: in march 2000, 2 years after her husband's death from colon cancer, tv anchor katie couric began a well-publicized crusade

to increase the number of peoplegetting routine colonoscopies, which can detect the disease in its earliest stages. so far,i'm looking pretty clean. so far, you're very clean. people don't wake up one day and all of a sudden have a cancer. you have this giant window of opportunity, 20 or 30 years, to catch a cancer before the final stages, which only occurs in the last few years

of this long lifetime of the cancer. and they can almost always be cured by surgery alone if they're caught early. ok, katie, that's it. that wasn't bad at all.no. partially as a result of couric's efforts, colon cancer screening is up sharply, and mortality from the disease is down nearly 10%. man: the full examination requires 3 views.

the craniocaudad view, the mediolateral view, and axillary view. narrator: in the 1950s, a doctor at the md andersoncancer center in houston, invented a method of taking detailed images of the inside of the breast. man: the head is turned to the contralateral side. the tube is then swung into place. narrator: the mammogram

was hailed as a major breakthrough in the fight against breast cancer. man: this is the finished product. note the second carcinoma within this breast not appreciating clinically. narrator: over the years, with the help of an activist breast-cancer community, the test became part of millionsof women's annual check-up. every woman in america over 35

should know this word-- "mammography." it's a fast and simple procedure that can detect breast cancerearly while it's highly curable. [cheering] we have pushed for mammography screening for once a year for a lifetime. early detection saves lives. whole organizations were built around that concept.

the breast-cancer industry was built around that concept. narrator: but like so many cancer therapies or prevention methods, the mammogram has turned outto be too blunt an instrument for the complexity of cancer. a bevy of recent studies have shown that while annual mammograms result in a clear reduction in mortality

for women over the age of 50, the benefit to younger women is negligible. in these earlier years, the test is too imprecise to distinguish a real cancer from a harmless growth. meanwhile, false-positive diagnoses have led thousands of women to undergo painful, expensive,and disfiguring treatments like mastectomy. in breast cancer,

we're so afraid of missingthat one patient in a thousand that will die of the disease,we end up treating all thousand. so that triggers enormous amount of procedures, treatments, interventions that is difficult to stop. it's ethically difficultto stop and economicallyis difficult to stop because the incentivesare to sustain it.

narrator: men have not beenspared the collateral damage caused by an imprecise method of early detection. like the mammogram,the test for prostate cancer, the prostate specific antigen or psa, is often misinterpreted, leading to high rates of false positives and unnecessary surgeries. the difficulty that's faced by the patient is saying, "is my early abnormality harmless?

or is it going to be harmful?will i regret not proceeding?" and that's a very difficult choice, because the consequences of being wrong can be devastating. there we go.right there. what we're all looking for is can we find markers that say, "yes, there's some abnormality, "but the likelihood of this developing into a frank cancer

is extremely low." narrator: these markers, or clues to the presence of cancer, might come in the form of mutations that turn up in routine genetic screenings. it's our hope, maybe our dream, that one day, when people go to their yearly office visit and deposit samples of blood and urine, et cetera,

these specimens will be tested for mutations. they will be alerted to the presence of... of a cancer which they wouldn't yet know about 'cause it hasn't caused symptoms, and they can then be handled through surgery, and the cancers are gone. that's the hope.

c-c-c-t-c-t-c-a... narrator: already, there are a few tests that can detect genetic mutations that will likely give rise to cancer before a single cancer cellhas even appeared in the body. the first grew out of the work of a young biologist named mary-claire king, who, in the mid-1970s, began investigatingwhy there were some families

in which breast cancer was much more prevalent than in others. i said, "this is a common illness. "how much breast cancer would we expect to see "clustering in families just by chance "because it's common? "and then, how much more or less than that do we actually see?" narrator: king discovered that in some families,

the rate of breast cancer was so high, it could not be by chance. she hypothesized that these families must carry a genetic mutation that they pass downfrom one generation to the next. to prove that there was a gene, and then to find it, king was going to have to work closely with affected families. i needed families who would be part of this,

who would be patient and who would be willing to have me come back to them and talk to them over and over and take blood samples and ask to collect the tumor samples when they had surgeries and would listen to my hypotheses and talk to me forever. narrator: there was one man she knew

who could help her find such families. dr. bernard fisher was, by that time, in the midst of his groundbreaking study on the effectiveness of the radical mastectomy. if anyone could introduce king to families with inherited breast cancer, it was he. meeting bernie fisher changed my life. he knew from his practice that these families show up from time to time,

and he knew that when he was working with a family that had had historically in generations 4 or 5, 6 cancers, he was sure that in the next generation, it would show up again. so when i asked him if he would help me identify families, he said, "of course." on this pedigree or family tree, circles represent women,

squares represent men, and filled symbols represent cancer. narrator: working in this way, family by family, king was able to identify the section of dna along chromosome 17, where the mutated gene was found. the gene was called brca. women who carry the brca mutation, which can be detected by a simple blood test,

know they have up to a 70% chance of contracting breast cancer and a 30% chanceof developing ovarian cancer. with this forewarning, they can take preventative measures. they can watch themselves more closely or choose to have their breasts removed before cancer ever appears. by knowing much more about how cancer develops,

doctors may be able to assessthe risks for each person long before he or she contracts the disease and develop strategies to prevent it or detect it early. i think the time will come where your ownindividual risks are going to bebetter predicted by usingyour family history, by using your own sort ofenvironmental exposures

and your lifestyle,and by using your dna. so here's not looking ata cancer genome here. looking atyour constitutional genome and saying, "ok, for you, "your risks of this diseaseare higher than the average, for that disease are lower." clearly, if we'retalking prevention in a way that's going to work,it can't be one size fits all. it's got to be focusedon that individual.

narrator: the combination ofprevention, early detection, and some new targeted therapies have made a significant difference in the fight against cancer. in the united states, cancer mortality has been slowly declining, down 20% over the last 2 decades. and there is optimismthat this trend will accelerate. one major reason

is that researchershave begun to discern patterns within the complexity of the cancer cell that once had seemed so daunting. the first step was understanding that not all the mutations in cancer cells are equally significant. most mutationsin a cancer cell are random,unimportant mutations. there's a limited numberof those changes

that really conferthe properties on the cancer. what we have right nowis a sifting process to find, by comparingmany different cancers, which ones arethe recurrent targets that really matter and givethe cancer its properties. narrator: those mutations thatare significant, it turns out, often play a key role in many different cancers. in fact, breast cancer and leukemia, which look completely different under the microscope,

may actually share some altered genetic components. so therefore, the world of cancer, having been diversified, now begins to find these-- and i can only describe themas sort of genetic wormholes-- you know, from one cancer to another. narrator: these fresh insights have rejuvenated the field of targeted therapy. if the many mutations in a cancer cell can be narrowed down to just a few,

blocking their effects might be possible with a technique already used,in a much less precise way, in chemotherapy-- combinations of drugs. the key is to hit a cancer with multiple drugssimultaneously. when a cancer mutates,it gains some new properties, but very often, it gainsnew vulnerability as well. it gains a power,and it gains an achilles heel.

so what's exciting right nowis that cataloging, for every mutation, the achilles heelsit creates. if mutation here, vulnerability there.attack there. might mutate, but you'vealso got over here to hit. you're laying out essentiallya way to deploy your armies, knowing that cancer's going to try to escapedown this path,

and you've got somethingwaiting for it. narrator: not only have cancer researchers narrowed down the number of oncogenes and tumor suppressor genesthat actually cause cancers, they've also discovered that none of these genes operates in isolation. instead, they work aspart of groups called pathways to accomplish specific tasks. there are only about 200 genes

which are responsible for the vast majority of cancers. then these 200 genes funnel down into only about 12 pathways. if you can figure out a way to target these pathways, you will have a therapy that's useful for many different kinds of cancers. you can think of a pathway like a circuitor bucket brigade.

if you disruptthe bucket brigade at any one number of positions, you could disruptthe entirety of the brigade. what we're learning now is that there may bemultiple different ways to activatethis bucket brigade causing cancer, but it also means thatthere are multiple places to intervene and disrupt it.

make no mistake,this is complicated. it's least as elaborate as the most complicatedelectronic-circuit diagram that you have ever seen. but getting our mindsaround that, even if it's somewhat imperfect, offers a lot of opportunities. narrator: with the cost of genetic sequencing plummeting, it may be only a matter of time

before doctors can map all the genes and pathways inside every patient's cancer and treat each of them with a personalized combination of drugs. where we're goingis this much moreindividualized approach, just like infectious diseases. if you have a very badinfection, very bad, your doctor willtake a sample of the bug, grow it, and pick an antibiotic or 2 or sometimes 3,

mix them together,and hopefully cure you. and that's what we'retrying to do in oncology now. narrator: no matter how powerful or precise, however, combination targeted therapy still must confront cancer's complexity and its relentless drive to adapt and survive. to me, the best wayto think about cancer is that it is literallyevolution in a bottle. it's like taking the enormity

of the power of 3 billion years, unimaginable timeframes, that have created the unimaginablediversity of life. imagine capturingall of those forces within a single cell and putting that insidesomeone's body. that is, to me,the metaphor of cancer. it is all ofthe history of life

that plays out at a billion times the speed of evolution. narrator: if cancer exploits the power of evolution to survive, perhaps only a commensurate weapon, equally adaptable and also perfected over millions of years, can overcome it. that weapon, many scientists believe,

is the human immune system. the immune system is an extraordinaryset of defenses, an intricate interplayof cells and proteins. they're circulatingthrough our bloodstream. they have these surfaces that keep looking and saying, "is theresomething foreign? "is there something changed?

"is theresomething different? because i have tokeep that out." narrator: the idea that the immune system might effectively treat cancer is not new. it was first exploredby a 19th century surgeon-- william coley. while working at memorial hospital in new york city, coley came across a strange case-- a patient whose tumor seemed to vanish of its own accord

after a serious infection. coley thought, "there's a power here. "we don't know quite how to harness it, "but i'm going to try to infect people "who may have this kind of dire, "inoperable form of cancer and see if we can do anything about it." and that, in a messy and unscientific way, was the birth of kind of cancer immunotherapy.

narrator: coley made a compound of infectious bacteria and injected it directly into the tumors of patients, hoping to trigger a fever that would somehow overwhelm the cancer. some of his patients were cured, but no one was able to duplicate his results, and for decades, immunotherapy remained on the fringes

of cancer research, even when scientists were ableto detect mysterious particles that appeared to be fighting cancer cells. man: we noticed these peculiar little bodies with the cancer cells. we don't know just what they are, andwe don't know what it means, but once the cancer cells develop these spots, they go on to disintegrate and die. well, that's it.that's what we've been seeing.

the little dots may be evidence of an immunological mechanism, or they may be something non-specific, and we hope we can find out with further study. narrator: immunotherapy remained a backwater, but a few scientists, certain that there was something to it, kept the field alive. one of them was steven rosenberg,

who, since the 1970s, has been exploring immunotherapy treatments at the national cancer institute. a surgeon like coley, he too had had a patient whose cancer had miraculously disappeared. all aspects of his cancer were gone. he had undergone one of the most rare events in all of medicine.

he had had a spontaneous regression of all of his metastatic cancer. narrator: rosenberg believed that the explanation had to lie in the patient's own immune system. he decided then and there to focus his research on immune cells or lymphocytes. ok, let's talk about admissions for--for this week. the body has hundreds of billions of lymphocytes. and somewhere in the body of a cancer patient,

there are lymphocytes, we hypothesized, that could recognize what was different about the cancer. so, mark, let's hear about-- let's hear about cells. i have cermak on the nma armof the randomized protocol-- rosenberg, voice-over: it was that hypothesis, it was that dream, that then led us to try to identify the actual cells that were attacking the cancer and use them to actually develop a cancer treatment. narrator: rosenberg isolatedvarious types of immune cells

in his lab, and in a series of clinical trials, injected them into patients. but progress was painfully slow. in the first 66 patients, his therapy showed no signs of working. then, in 1984, he treated the 67th-- a navy officer named linda taylor-- with a far higher dose.

3 decades later, she is still in perfect health. aw. i tell you, i never cry except around you. i know... rosenberg, voice-over: it was an important event in the development of cancer treatments because it showed people that it was possible, at that point in a very tiny percentage of patients, to cause the immune system

to make a cancer disappear. the hope from those early experiments was that if you could somehow activate specific aspects of the immune system, could you now educate it to attack a cancer cell and not attack a normal cell? narrator: rosenberg went on to discover that a specific type of immune cell

called a t-cell was active against some cancers, but when greatly outnumbered was too weak to defeat them. through dozens of experimental trials, he learned to extractthese cancer-fighting t-cells from a patient's own body, grow them in the lab into a vast army billions of cells strong, and then infuse themback into the patient's body

to fight his or her cancer. so, naomi, you have 68.6 billion cells. more than what you thought. narrator: rosenberg is running several clinical trials for melanoma patients using this approach. all right, dear.right here,little buggers. right in this area.chew, chew, chew. narrator: every week, he sees a new group of patients,

all with advanced cancers, most of whom have exhausted every other treatment. mr. rogers,i'm dr. rosenberg. hi. delighted to meet you. good.please stay right where you are. i'm jan.jan,delighted to meet you. tell me, when did youfirst notice a problem? september of 2011 when i had a mole... narrator: doug rogers is a 60-year-old retired nascar mechanic from south carolina.

he found out he had metastatic melanoma when he had a black mole on his leg checked in 2011. and then right in the concave area where the mole was, a little black crusty place came back up. narrator: the cancer soon started taking over his body. so show me where the- where the tumororiginally started.

where was the original molethat you had? right here. see the scar? i see. i surely do. yes. ok, good.you can lie back. what we have to doto perform this treatment is we have to take offone of the tumors because we have to isolatethe immune cells that are actuallyattacking the cancer, and what better placeto find them

than withinthe cancer itself? and we grow them up, and thenwe give them back to you, and in other patients, we've seen very remarkable disappearance of cancer. so that's whatwe have planned. i've gone over your x-rays.you seem to be a good patient. now this might be a little chilly. i'm sorry about that.

narrator: 2 days later, the team prepared for an operation to remove one of rogers' tumors so they can find the t-cells that may be trying to fight it. so this operationis going to be pretty simple as far asanesthesia's concerned.got any questions for me? no, sir.all right.where are you from? i detect a little accent. brooklyn, new york. wife: that's no accent.

that's a drawl. south carolina. wife: we've been together since i was 18. and i'm 55 now. we've traveled down a lot of roads, so we've just got a lot left to do together, and we got to beat this. are you feeling it? bye, honey. might not remember this part. love you. this may lengthen his life or even cure him.

i can't wrap my brain around being without him. it just--i can't do it. you know, he drives me crazy, just like any husband drives a wife crazy, but, um, i can't imagine life without him. narrator: with rogersstill in the operating room, rosenberg's team delivered a sample of his tumor to the lab.

rosenberg: in the laboratory, one of our technicians is waiting to dissect the tumor into tiny fragments, put those fragments into individualculture wells and let the lymphocytesgrow out of them. narrator: over the next 4 weeks, rosenberg's team will nurture rogers' immune cells, trying to turna few cancer-fighting t-cells into an army billions strong.

rosenberg has not been the only scientist investigatingthe immune system and cancer. in the early 1980s, a scientist at the university of texas, jim allison, began work in the field, even though he was told it would stall his career. there was such skepticism about immunotherapy in general. i remember as recently as 2004

going to a meetingof cancer biologists and feeling that i probablyshould wear helmet and, you know, a body guardand everything to avoid being abused fr-from havingthe audacity to say, "i think the immune system can take care of cancer." narrator: allison's idea was very different from rosenberg's. instead of trying to boost the immune system, he thought the immune system

might somehow be holding itself back from attacking cancer cells. everyone was looking at ways to stimulate the immune system. no one realizedthat there were restraints or brakes. allison found that a certain protein acted like a brake. so you can remove the brakes,

and then the immune systemgoes to work. narrator: in 1996, allison developed a compound that could free the immune system to attack cancer. it took him years to find a company that would help him produce his drug, but when yervoy finally came to market in 2011, the whole pharmaceutical industry

quickly took note. since then, several new drugs have been developedbased on the same principle-- removing the constraints that prevent the immune system from attacking cancer. canceris a dynamic interplay between patient and tumor. and for many decades, we have concentratedall of our efforts

on the tumor partof that interplay. and now i think we recognize that there is a roleto be played by focusing on the patient and how this hostimmune response can be tuned to tryand control the cancer. narrator: what makes these new immunotherapy drugs so exciting is that, unlike rosenberg'shighly customized treatment,

they can be mass-produced and administered at any hospital. the fruitsof jim allison's work moved the fieldof immune therapy to make it generic. and that has tremendous impact. from a financialpoint of view, you don't needto individualize. you have the same vialfor everyone.

narrator: for reasons not wholly understood, immunotherapy has so far been most successful in fighting a small group of cancers, mainly melanoma and kidney cancer. for most other types, the cells in the immune system still seem unable to find and fight the cancer. but another novel approach may greatly expand immunotherapy's reach.

in philadelphia, at the university of pennsylvania, dr. carl june has used genetic engineering to give the t-cells in the immune system a kind of homing device. we know the immune system can be around as a form of surveillance and cull out the early tumors. but in most cases, it fails,

and it can't really distinguish at all between a tumor cell and normal cells. the t-cells can't see cancer cells. they are completely blind. they will wander right by. you can actually see this under the microscope. they don't recognize the cell as being bad. so we have to redirect that t-cell. we put in a new gene into the cell, and that new gene forces the t-cell

to see the cancer cell. so it's very much taking off the blindfold and allowing the t-cell to see the cancer cell. narrator: by re-engineering t-cells this way, june is creating a living drug attuned to each patient's cancer. he received approval to try the technique in a clinical trial ofseriously ill leukemia patients. at the same time,

a 6-year-old girl named emily whitehead, who was being treated for leukemia in a nearby hospital, took a sudden turn for the worse. our doctor come in and said,"she has a full relapse. "it's very different now,and, you know, survival is less than 30%." we found out that she does have a specific mutation, and the doctor told me not to google it,

not to look up any information on it. and so of course i did right away. and i saw that very few people with that specific mutation survive. i mean, very few. [machine beeping] narrator: emily's health worsened by the day, and when the possibility of a bone-marrow transplant fell through,

the whiteheads leapt at the chance to enroll their daughter in dr. june's new trial. you know, if anything was going to work, this was going to be it, because there wasn't anything else left for her. if it didn't work, we probably only had a few weeks left with her. narrator: while emily's family waited for her immune cells to be prepared, doug rogers returned to the nci

to continue his treatment with dr. steven rosenberg. you guys want to come overand see the lab... yes. we're looking forward to it. all right. narrator: a month after the operation in which his immune cells were extracted, they were nearly readyto be reinfused into his body. tomorrowwe're going to give you exactly one billion cells,

and about 12 hoursafter you have those cells, they're going to begrowing in you, and you're going to have2 billion cells. in 12 hours, my body will will double. i thought it wastruly amazing. yeah, it was. i mean, it was so interesting. and then letting me look atmy cells under the microscope. it was extraordinary. there they are.

it was really emotional, too. i caught myself just fighting back tears. i didn't want to embarrass myself crying over a little thing of dougie's cells, but, i mean, it could mean everything to us. i mean, if you could havelooked under the microscope, and all the melanoma dotswere gone. it was replacedby healthy cells. and then when he actuallylet me hold them... shaking.

look, you could see them all in there, if you look carefully. see them all? you're holding your cellsin your hand that might save your life. that's a lot of cells. feel it? ok, look this way, dougie. afraid i'm going to drop them. don't drop it. [doctor laughs]

got it. i'm just excitedto get them in there and let the cells... do their thing, huh? do their work that the doctors designed them to do, hopefully. narrator: the next day, however, there is a problem with rogers' cells. a virus has contaminated them, and they are no longer safe for infusion.

something very unusual happened to your cells, and that is, in the last day, it looks like they're infected. and so our plan is to abort the cell infusion today, of course, and prepare a new batch for you for next week. that's the bad news. the good news is that we have things in reserve.

can you grow themand prepare them in 6 days? we can. from everything i understand about what went wrong, we should be able to get you good cells 5 or 6 days from now. ok. obviouslywe were disappointed, but you can't do anythingabout it, so you just move on. you have to dig down deep and find your strength and just be prayerful that he'll stay healthy

for the next week while they're growing. and they were such good,healthy cells, too,they said. but, i mean, so will--these will be also because they came out ofthe same batch, so they'll be fine. might even be better. narrator: 4 weeks after arriving at children's hospital, emily's cells were ready. she would be the first child

and only the fourth person ever to receive this treatment. and her doctor, stephan grupp, prepared to give her the first of 3 infusions. man: ok. ok. emily whitehead--554... this is the stuff that we're actually talking about, and each day, the volume goes up. we've only done this in a very small number of adult patients, but how actually well it will work in kids

is only possible to know by actually doing it. all right, we're going to get started here. why's there 2 of them? you're seeing 2 rachels. that's all right. ok, we're done. that's the whole thing.mother: yay. yeah. so we finally got there. yeah.

it's a little bit less than we usually give, but this should be enough, and they're very highly potent. narrator:a week after doug rogers' original batch of t-cells was infected, he was given an infusion drawn from a much smaller batch kept frozen in reserve. it was the first timerosenberg had ever tried this. jan, voice-over: i'd be just lying if i didn't say i'm- i'm not terrified and--

what are y'all nervous about? i mean, sometimes we havethose hard conversations now, and i do fine with it until, like, night comes, and then it's hard. rogers, voice-over: hopefully,i got a new lease on life. my cells are saying,"let's get to work." they're rollingtheir sleeves up, see. got a voracious appetite,hopefully. and we envision themas pac-man, you know--

they're going to go to those melanoma cells. you ok? [groans] mother: what's the matter? nauseous in this one. day 2--we went inand got 30% then. first day was 10%. and we went home,she was on my back doing horsy-back ridesand, uh, felt good. and then at midnight,she spiked a fever,

so we drove back to the er, then things justspun out of control. and they put her to sleep,you know, and then that was tough,you know, 'cause at that point,dr.--you know, dr. alexis said this is as seriousas it can get. and then they had a whole team-- as soon as they had her under, a whole teamof doctors come in,

and i suited up with themand put the mask onand everything, and then, you know,watch them cut artery lines in both wristsand then in her thigh, and they cut an artery linein her neck, and when they were done, there was 17 i.v. pumpskeeping her alive. [dinging] they came to us and said that they didn't think

that she was going to make it through the night. i remember sitting by her bed watching--watching her on the ventilator, and i just kept thinking that this can't-- this can't be the end. this isn't how it's going to end. it can't be it. grupp: she's as sick as a human being can possibly be. the icu staff are working flat-out to try to keep her alive.

we obviously think this is a toxicity of the t-cells, but we don't really know what's happening. and so now what? narrator: with emily's life slipping away, june's team frantically rananother batch of blood tests, hoping to uncover precisely why her new immune cells had turned on her and made her so sick. the tests came backshowing skyrocketing levels of an immune protein called il-6.

when those levels came back, they were literally off the charts, and so then i suggested a drug that can block il-6. that's never been given to cancer patients before, but it is an fda-approved drug for juvenile arthritis. and it just happens that my daughter has that disease. dr. grupp said,"i'm going to tell you,we're grasping for straws,

"but if we give herthis arthritis drug,it could help 'cause she can't get any sicker,or she won't be with us." there is an enormous role of luck and happenstance in these kind of situations. we gave that drug, and her response was astonishing. i mean, the icu staff that were on that night say they have never seen a patient that sick get better that quickly.

narrator: emily finally woke up in the intensive care unit on her seventh birthday. after her brush with death, the doctors still didn't know if the t-cell therapy was working. 3 weeks later,they did a bone marrow test. it came back negative. emily's leukemia had vanished. ⶠi want to celebrate and live my life â¶

ⶠsaying ay-oh ⶠⶠbaby, let's go ⶠnarrator: emily's close call had threatened the clinical trial, but in the end, dozens of other childrenwith leukemia were treated... ⶠ'cause i told you once ⶠand the arthritis drug that saved emily's life became a standard part of the therapy.

emily was through the worst, but she was entering uncharted territory. as the first child ever to get this treatment, her medical team had no idea how long her new immune cells would be able to keep her cancer at bay. so in our last6 evaluable patients, there are 4 complete regressions and 2 partial regressions, so-- we're in the beginnings of a very long

and hopefully exciting road with immunological therapies. there are people who've dedicated their lives to this, and finally, we're beginning to see interesting glimmers in which the immune system can be educated uh, to--to-- to start to see cancers and to kill those cancers. narrator: right now, immunotherapy remains something of a roulette wheel.

this large one almostgone away completely,right? what is it like-- narrator: doctors are not sure why it works in some patients and in some cancers and not in others. wow. she's havinga fabulous response, is it? [overlapping chatter] it looks like everything has virtually disappeared, so we're thrilled for you. um, you know, likea little over a year ago, i thought i was going to--i was going to die.

but you've saved my life, and i just can'ttell you enough that-- to thank you just for--just everything. narrator: in rosenberg's most recent trial of 25 melanoma patients, 18 saw their tumors shrink, and 9 were still alive after 5 years. but for the others, there was often no further treatment he could offer.

why don't you measure it,would you? [mutters] looks larger. that one does look larger. it's 40 millimeters up to 48. rosenberg, voice-over:the patient comes forthis follow-up scan, and for them, this isa life-and-death visit. if the treatment has not worked, very often, there'snothing left to do for these patients. all right, let's go see.

[mutters] narrator: a month after getting his cells, doug rogers is back to see if they were working. well, hello again.so nice to see you. come over here and sit down. nice to see you again.hi. good to see you. well, how have you been doing? i'm doing good,real good, matter of fact. tell me what you've noticed about your, uh...

well, it just looksso much better, but mainly,it just feels better. i mean, it feels pretty muchlike my right leg does... i've been looking at your x-rays, and the x-rays show more than half of all the cancer gone. it's at least a 55% decrease compared to the start on the x-rays, both in the groin as well as in these tissues, so... jan: that's amazing. we're real excited about it.

so you had these 2 big ones. and those 2 big lesionswere these 2 that are now way, way down. yeah. well, that's really a good sign that things are happening so quickly. it was for me, but from your standpoint, are you pleased with everything how it's gone? you can--you can sit up now. again, when we see this kind of regression at one month, it very often continuesuntil everything disappears,

but not always,so we're going to haveto follow it carefully to be sure it doesn't start--it doesn't start coming back, see, so...just couldn't be more thrilled with how things are going, so... we are, too. thank you very much. sure. ok, now wait here 'cause dr. klein-- i want dr. klein to come in and just go over you a little more carefully. ok. so nice to see you again. we'll see you in a month. ok.

i'll see you in a month. i'll be here. absolutely. thank you very much. wow, that isfabulous news. 55%. [kisses] that's pretty good news.good news. but you've got to thank the man upstairs first. that's right. 55%. that's amazing. just thinkif it continues like that,dougie.

narrator: in april 2014, 2 years after she received carl june's risky gene-therapytreatment for her cancer, emily whitehead returned to children's hospital in philadelphia for a check-up. let's go up the steps quick. well, today is emily's2 years since treatment, so, you know, we're going toget her blood work checked and--so it'sa big day for us.

we're always a little bit nervous 'cause just walking into the hospital, and you hear the sounds that we heard for 3 months. there's that big structure,and there's, like, a dinging, and all of a sudden, you know, it'll hit us all over again. there's been too many timeswhen we didn't getthe right outcome, so it does make us nervous, but we don't expect anythingbut good results today.

how about it, em? what do you think? how you feeling? good. any problems? no. none whatsoever? no. you go to schoolevery day? yes. do you listento your teachers? yes. ok. how are your grades? good. when we wrote this trial, we said we would follow patients for 2 years.

we never imagined that we-- i would actually be able to follow patients for 2 years, but we said that's what we would do, and now we've reached that point. nice deep breaths. we'll continue to monitor her situation. we'll continue to watch for the possibility of her disease coming back. but she has completed the treatment. the questionyou're really asking me is, how long do you need the cells to stay in remission forever?

and the answer isi don't know. yeah. you know, we're super excitedthat she's at this point-- dad: we are, too. but, you know, every day that she goes out fromher cell therapy makes her unique, so, you know,amazing thing is that she's doingas well as she's doing. the nerve-racking thingis we don't really havethe answers on what's--the next yearor 2 years or 10 yearslook like.

we don't know'cause she-- she is plowingnew ground here. you know, nobody thoughtwe would be in this positionwhen we started. i have a dog, a bunny and a fish. oh, my gosh.you love animals, don't you? she is absolutely a pioneer. i mean, she was the first kid. she was the first patient with a.l.l. she was the first patient who got so terribly ill.

she taught us about the toxicity control treatment which has saved this therapy. all right, so let me set this up real quick. turn on the lights. we've now treated 30 children, and had, you know, 27 of them have complete responses. i mean, they're not lasting in all of them, but-but, um, it looks very hopeful that there's going to be many more children like emily.

we can't say the "c" word, cure, yet. we don't know. it's only with more time will we know if every last cancer cell is gone. we got some results back,and, um, cbc looks good. uh, white count's 4.5, hemoglobin's 12.9,and her platelets are 171, and the differential's ok. so the preliminary lookis 2 years cancer-free, so, uh...

it's a good day.it's a great day. yeah. narrator: so many promising cancer cures have come and gone over the years that many researchers remain cautious about the meaning of this latest development. but results like emily's have made immunotherapythe talk of the cancer world. early results are raisingthe tantalizing possibility that we may actuallybe seeing cure.

it's too early to tell 'cause to know you have a cure, you're going to have to wait,but it has that feeling, and i thinkthat's why there's this literally a thrillgoing through the entire oncology community to see some of theseclinical responses to these new immunotherapies. what was unique in our experience was that most of these responding patients

achieved deep or complete responses... we have seen that with targeted therapies resistance occurs, but here is different. this immune system is not taking any vacation. that immune system is there for the whole trip. the patients that respond to immune therapy,

they respond for a long time. and i think that this will change clearly the way we treat cancer forever. narrator: it seems unlikely that any one treatment or method of prevention, or all of them working together, will ever eliminate cancer completely. the history of the struggle against the disease, from medieval apothecaries

to modern operating theaters, from radiation to chemotherapy to targeted therapy and advances in prevention and early detection all have taught the cancer world the value of tempered optimism. but no one doubts that the great barrier to all cancer therapies, the mystery of how cancer works,

is finally being broken down by the concerted worldwide efforts of researchers and doctors and nurses and by patients. fresh insightsfrom the cancer genome atlas are revealing in ever-greater detail the nature of cancer's complexity, enabling researchers to uncover patterns in the ways it evolves,

interacts with the immune system, and thrives inside the human body. this profusion of knowledge is inspiring new ideasfor treatment and prevention. while scientists are reluctant to use the word "cure," many believe that it is only a matter of time before most types of cancer become manageable, no more terrifying or destructive than any of the other chronic diseases

that afflict humanity. ready, set, go. whee. we have entered a time that is incredible. 1, 2, 3. our understanding of cancer is really at a point where we have the opportunity to make progress

at a rate and a level that we've never seen before. hands together. bat right here. let your arms come straight out when you swing. see? see there? there has been one revolution. that's the revolution in understanding the disease. pop gets an at-bat. the second revolution, which is taking that understanding

and putting it to work for us in cancer patients, is a work-in-progress. uh, it's not going to come quickly. it's not going to come without research, uh, but it's going to come. you look so pretty. where are those fingers? [giggles] there they are. when you look atwhat's going onwith cancer right now,

it's stunning.it is exhilarating. i'm amazed that we can,in the course of half a century, go from knowing nothing to understanding a problem, to developingrudimentary solutions, to better solutions, to whole armamentariumof solutions. if it takes half a century,and if it takes a century, that will still bean amazing triumph,

and if it's therefor my grandchildren, that's nothing we shouldbe apologizing for. what i'd like to see you do is first to localizeyour lesion... there are critics who've said that we're caught in this perpetual cycle in which we have hope and then despair, but these cycles have moved us forward. come back.

the way that we've understood and treated cancer as a biological entity, as a-- as a social phenomenon, as a cultural phenomenon has transformed over the last few decades and will continue to transform in the future. fantastic. wonderful. if the cancer cell is evolving, then so are we.

announcer: for web-exclusive content, more about the film, and to watch the entire show, visit pbs.org/emperorofallmaladies and join the conversation on twitter using #cancerfilm. "cancer: the emperor of all "maladies" is available on blu-ray and dvd.

the companion book is also available. to order, visit shoppbs.org or call 1-800-play-pbs. also available for download on itunes.