off on tangents and have enough time to really explore. up next, jessica wapner come author of "the philadelphia chromosome" talks about the discovery of a mutant, is owned by a scientist in 1959 and the eventual realization decades later that the mutation is the cause of a certain kind of leukemia. this led to the first ever successful treatment of cancer at the genetic level and opened research.field of cancer

this event hosted by the powerful city of books in portland oregon is just over an hour. >> hello. always nice to start with a hello. it's great to be here. i am thrilled to be at powell's speaking. i was last here in portland a year and a half ago to interview brian when the act actually writing the book seemed like how is this going to happen? so it's wonderful to be back. i'm glad it's not the be ready this time and it's just great to see everybody here. so, i am going to read you an excerpt from a book just from the very beginning so i'm not giving anything away. and talk with you a little bit

about why i wrote the book, why i think the story matters and why i feel that needed to be written. why i think it's important, because of its eternal important qualities. and also why now, why the story at this time and then we will have time for the q&a as you heard from the doctor. okay. so, i will begin with the excerpt from the pre-lewd which is entitled down to the bone february, 2012. garre the eichman sat down in a chair backed up against wall. across the room, his nurse was half hidden by a computer to read she schools through his medical chart on a monitor he couldn't see typing his responses to her questions.

he answered and smiled as if he were just fine to get as though that would somehow make it so pity he kept his worry concealed, silently wondering what the next hour would reveal about the disease that had suddenly overtaken his life. if year permeated his every thought. the nurse ran through the litany of side effects that he might be experiencing from the leukemia medication he had recently begun to take. any chest pain, she asked, heart problems come any swelling in your ankles, any problems with nasea? he had massive cramping and pain in the stomach he told the nurse. it's like the worst thing that you've ever had. the nurse knew that he really had no idea of the worst thing

someone with this type of leukemia could have. few patients with this disease today will ever know that kind of pain. but as the nurse was taking anything of the sort she kept to herself. after all, her patient was about to have a large needle inserted into his ballan so that his doctor could extract a sample of narrow. having witnessed countless procedures in the 12 years she had been a nurse to the patient taking the drug she knew how much was riding on this biopsy and she knew that he was well aware that his life was at stake. if anyone could set him at ease it was his doctor, brian druker. all i care about is that you are making some progress and he told his patient who had come to the clinic in portland oregon for a bone marrow biopsy. the procedure would reveal whether the medicine, the till

he'd been taken daily for six months was tackling the leukemia that had invaded his body. he had a chronic leukemia to a cancer of the white blood cells that the slow-growing could be fatal. i will be happy if you are 18 out of 20. he nodded his understanding and his foot the only sign of his nervousness. for mike mur those or part of the language that he had learned since his diagnosis in the summer of 2011. as with so many cancer diagnosis the education began suddenly and unexpectedly. after a day or so of sharp excruciating kidney pain, the single parent of a teenage boy drove himself to the emergency room at the local hospital in columbia washington where he had been living at the time. his sister-in-law told him she

thought he had kidney stones. so the mike mur was expecting to be admitted free standard albeit painful procedure. but when several doctors balked and the hospital room together, he knew something wasn't right. you don't have kidney stones, they told him. you've got what we believe is leukemia. a blood test soon revealed that i eichner had the number of cells contained in a sample that confirmed that much. the doctors explained the stabbing pain he thought came from his kidneys probably was from his spleen enlarged by the high concentration of the cells, although the slow-moving nature of the disease meant he wasn't in immediate danger there was not any time to lose. for the best chance of long-term survival, he needed to start treatment right away.

as he was rapidly informed common danger could eventually come. if the treatment didn't work, within five years his bone marrow with phil come of the white blood cells that failed to mature with overly abundant and useless. his blood once free-flowing what turned into this. the supplies of the iron a rich blood that carries oxygen around the body with steadily plummet, leaving him fatigued and anemic. it would render his blood unable to clot. as the disease progressed the minuscule capillaries leading to his eyes and his brain with clogged. his spleen would likely become profoundly enlarged as his body began shutting down he would leave in his brain and his intestines and out of every orifice. two days later, she was having

his first bone marrow biopsy performed by members that spoke broken english to hammer in the 4-inch long needles to break through his bones which have become hardened and enflamed. finally, she managed to extract an ounce of marrow the spongy matter in the center of the bones where new blood cells are made and the genetics laboratory of the fluorescent dye that is played to the dna in sight of his blood cells retial the sign of cml a genetic mutation known as the philadelphia, some. an abnormal chromosome regarded as the defining feature of this fatal and spontaneously a rising cancer and discovered more than 50 years ago. contained to this genetic error.

they told him to call the doctor named brian and right away. don't do anything before you see him come he told him to be the had a call who mysteriously he didn't know exactly how he'd gotten his phone number. during the next 20 minutes to talk him down from his panic assuring him that being in the early stages of the disease. they were making the trip south to the health and science university where they've been treating and researching leukemia since 1993. he gave him his professional blessing to go drink beer. it was august and he'd been getting ready to leave for the day at the annual summer fast.

he was on his light portland within three weeks of his diagnosis he was swallowing his first public of medicine of medication which he had been instrumental in developing. a drug aimed at tackling the cancer at its root. so i will leave you in suspense. garrey is still alive and was supposed to be here. i was hoping that he would walk right and after the excerpt. so, yes, six months after he began taking the drug that i write about and his test came back zero out of 20. so you remember i said when he was diagnosed he was 20 of 20 meaning in the sample of the cells taken from his bone marrow, 20 of 20 contained a genetic mutation called the philadelphia chromoso. so six months later it was zero

out of 20. so i would like to start with that excerpt that shows so much about why the story is important and why i love it so much. because of the impact the scientific progress has on our lives and this unstoppable drive that we have to make tomorrow better than yesterday. and the link that people will go to ensure that progress happens. when i first began researching the story i didn't know that it would be like this and i was working at a medical journal in the year 2000. and then heard the philadelphia, some when data was emerging from the studies to be i didn't know what it was the name was very captivating. was a great name for a genetic mutation, "the philadelphia

chromosome." years later i became a free-lance writer and wanted to dig and a little bit more about the story to understand what was it, maybe there was a magazine article that i could write about it. and i started talking to some people including brian druker and the people i knew by that point. my research began with the question why was it called the philadelphia chromosome. it's named after the city where it was discovered in 1959. to scientists were researching looking through a microscope through all different cells. peter had studied across this method for expanding cells more than they had been expanded before. and because he was in a hurry he was very anxious to cure cancer. he was young and ambitious and he thought he could do it in the

summer so he rented under tap water instead of the special laboratory water to it and suddenly, he could see the chromosomes just a little bit more than people had been able to see them up until that point. so we have today what was quite course. he wasn't interested in chromosomes. there was no knowledge about the connection between the genetics and cancer. nobody was looking for the cause of cancer in our genes. ..

one of the chromosomes was a bit too short. he was one of the handful of people probably in the country, if not the world, who could have spotted this at that time, and what he saw is actually on the cover of the book. obviously much tinier what he saw but it was this. okay? chromosome 22. and this cell sample was a bit too small. they didn't know what to make of it at the time and there wasn't any technology to figure out

what was going on, was the cancer causing the mutation or was the mutation causing the cancer? was it just along for the ride? so that was my first entry point into this story. but then, as i began researching the science and understanding how this became unraveled, how the philadelphia chromosome did turn out to be connected to cml. the twists and turns of the science, i thought it needs to be written down and i'll give you an example. okay? so, we have in our cells a protein called kinase, a type of enseam and sets things in motion. and one time of kenase tryingers production of white blood cells.

and our bodies don't always need to be making wide blood cells so the kinase is sometimes giving the signal and sometimes not. the redlight and green light. that's the normal kinase. but with the philadelphia chromosome mutation, the kinase that triggers the production of blight blood cells to be mutated, and in the mutated state it goes hay wire and always tryinges the production of white blood cells. it was a constant. so i wondered how was it known that knase were even involved with cancer, and i spoke with ray ericson, the first scientist to find the involvement of kinase in cancer. i said, why were you researching that? he says if was researching actually a gene call sarc and

looking for the protein products of the gene called src. and i'm, let's src? he said that was a gene involved in chicken cancer. why were you researching chicken cancer? used to get made fun of for doing that in the 1970s, and the story went like this. src was a gene involved in a virus that caused cancer in chickens, and when they went to fine out, how did it cause cancer in chickens, is when he uncovered the role of kinases, and where that gene had first been found was when -- went all the way back to 1910, and this is just to give you an example of the twists and turns, how we just never know where science will lead to or where it has come from for that matter.

this is a true story in 1910 there was a scientist peyton rose who was researching at rockefeller institute, now rockefeller university in manhattan, and he had gotten there in 1909, had been researching for a year, and one day this woman shows up at his lab, carrying a chicken. with a tumor sticking oust its belly. and the true story, she says she walks up to this lab and says, can you operate? can you operate? well, he says, sure. okay. why not? so rockefeller institute had its first if chicken surgery. so he removed the tumor from the hen. unfortunately the help did not survive. the was remnants of the cancer in its body and it died. now peyton rose had this tumor

and figured i've got to research this. i'm not going to waste this. so, he creates an distract -- extract from the tumor and injects it into another chicken, and the chicken got the same cancer as the first one. ah, contagious. contagious chicken cancer. what is important.the story is not that rose discovered contagious chicken cancer, which is very fascinating, but that research eventually led through the research of src, eventually led to the understanding of the underpinnings of cancer, it can begin in our own genes. the culprit gene in the chicken virus had come from the chicken itself and that is what led people to understand that our --

it can happen in us. if you think about is, just a preposterous notion. how would and why would our healthy dna undergo a mute addition and in that mutated state, trigger something that kills us? and i just -- i love that story to think that our current understanding of cancer goes all the way back to this farmer who brought her chick top -- chicken to a laboratory to undergo surgery. first of all it would never happen today. the paperwork alone, she would just say, don't need theicken. right? so, the science was very interesting to me. but then it was when i started to understand what happened next that i thought, you know, this has to be a book. this is more than an interesting

story. because in the 1980s, when the picture became clear about how the philadelphia chromosome leads to cml, which i described to you, there was some people who started to think, well, could we make a drug that targets that? right? could we make a drug at that time blocks that haywire kinase that stops the cancer at its root cause? this tip of drug had never been attempted before, never even really been thought about before. and one of the people asking that question was brian druker, and we work with people at the time in the pharmaceutical company at the time, it in switzerland who were also asking this question, could we make a drug to block the cancer at its root cause? and after working at the

chemistry for a couple of those years, which is a fascinating center its own right and i would turn you into a chemistry lover completely. they had a few compounds and sent them to brian druker in portland to test in this laboratory. they sent him five and they didn't tell him which one was the one they thought would work against cml cells. so heted them in the lab and investigate away could see one of them as carrying the dml cells show. gave them to his students. tell hmm which was the one, and the same thing happened. so, you would think, having seen that result in a laboratory, that the farm -- pharmaceutical company would move rapidly to the next step. having seen such promising work

in the lab, the next stepes animal stud studies and if it's proven safe, human studies, right? but everything gro to a halt. and i wanted to know why. i wanted to understand what happened. because this compound came so close to not being made. and i wanted to know why was it, how could it be that a life-saving drug was almost shelved. there were a few things i found out and i'll talk about a little bet of what i learned. first of all, there was the risk. i told you this drug had never been made before. and never been attempted before. and it was risky. it really was. because if the drug ended up

blocking more than one kinase, as one of the investigators on the first study put it to me, that was going to be one sick patient. it was risk. you don't know what going to happen when you give it to people. tragedy, disasters like what happened with thalimidt. this ended up deforming babies and whether that -- nobody wants an event like that to occur, and the checkist who made the compound that would eventually be called gleevic, said you can look at this drug and say why cooperate -- couldn't get it to

faster but if something happened you would say, why diddous risk it? how can you do that? which i thought was a fair point. and there were problems. there was a point where the drug -- the drug was tested on animals. moved into animal studies after some delays, and it was tested on mice and rats and dogs and rabbits and monkeys and hamsters, and some other cell lines, and there were problems at one point in dogs. some dogs were experience liver toxicity, and bryan druker got the message there were toxicity problems. they were not sure whether the drug would move forward. a man named alex matter, a drug company, leading the drug development program at the drug company, what hearing from a toxicologist who was conducting the animal studies, telling him,

not over my dead body will this compound go into man. but brian druker is saying, okay, there's live toxicity in dogs. fine. but you have to give this drug a chance. you're giving dogs 600-milligram doses of the drugs. a clinical trial starts out at 25-milligrams. and we know the size of liver toxicity. we're doctors. that's what we do, and in a clinical trial, that's the best healthcare a person can get in a clinical trial. irthere's a problem happening we'll see and it stop the drug. we won't keep giving it until they have extreme liver toxicity. give the drug a chance. but that wasn't the only problem. okay? the other issue was the money.

cmo is a rare disease, diagnosed in about 5,000 people per year in the united states, up to 75,000 people per year worldwide. so, to give you some perspective on that, breast cancer is diagnosed in 230,000 people per year in the united states. all types of cancer, 1.6 million people per year in the united states. so, 1.6 million, 5,000. the drug company could not see how they were going to recoup on the investment. the patient population, or the market, as it's called, was too small. and they were looking at that through the eyes of a -- through the business model of chemotherapy, which is given for short amounts of time usually, right in so they couldn't see how to recoup on its investment.

so, eventually the drug did good into a phase one clinical trial that started in 1998, and the results were stunning. in the clinical trial that is only supposed to be testing for safety, patients were having incredible responses. 100% of patients had a hem tollingic response. blood counts returning to normal show. normal range of white blood cells is up to 10,000 paints. parents with cml could come in with counts up to 100,000, and after a few months on the drug were back in the normal range. it was unprecedented. but even after the face one study, even when those results were coming in, this were still delays, when it would move from phase one to phase two because all of the doctors conducting

the study are saying, we have to get this drug to everybody. right? every cml patient who wants this drug should have it and should have it now. there were still delays. so, -- actually, this is one of my favorite moments in the book. there was a patient named susan mcna -- mcnamara and when the phase one trial was going on it was perfectly time with the rise of cat rooms. cooperate have -- couldn't have been better timing. so cml patients, 0 find support to find others going through the same thing you're going through, it wasn't -- it's a rare disease so you're not going to find many anymore your town in your city,

with this disease, but online there was a whole community to be found of people going through what you were going through, being treated with interferon, the primary drug given to patients with cml, which is a very, very harsh drug, very harsh drug. or having been through a bone marrow transplant addition, another harsh procedure. the only technical cure for cml, if you survive it, which is a 50% chance. and if you're eligible for it and if you can live with the side effects which last a lifetime, or can last a lifetime. so susan mcnamara was very sick and basically living between her bed and her computer two feet away, and she would go on the cml chatrooms and be reading reports from people in the clinical trials posting

about how great they felt that their blood counts were back to normal and they were having incredible results phloem drug. so she e-mails brian druker and asked to be but on the study. and he said he would put her on his waiting list, and it was 2,000 names long, and he had to choose who was the sickest. so he says, i'll put you on the waiting list but i have to tell you, i don't even know whether this drug is going to be made. i don't know when the trial will open in an expanded kind of way. just don't know. maybe you can do something. and she told it to me. she said, you know, at that moment i just felt there was no way that there was a drug in this world, that there was something that could help me

that it was not going to get. and she wrote a petition, signed by hundreds of patients within weeks, sent to novartis and very soon afterwards the phase two trial opened, to many hundreds more patients. and that just scratches the surface of the many heroic moments, the tragic moments, the frustrating, blood-boiling moments in the story, that i just felt, this needs needs to e told. because in -- in part because this is an origin story for this current moment in cancer research, where we are learning so much more about the link between genetics and cancer. in part because it pulled back the curtain how medicine is

made, on the science that goes on, the politics that can go on to equip ourselves with the knowledge so when we as healthcare consumers think about the world we live in, we know -- we know the facts of what goes on. but also, not only to tell the story of this miracle drug, but also to tell the story of the mr. rackous helpings people go to make sure they get a chance in this world so i wrote the book. and that concludes the talk portion for now. thank you so much. and i will invite brian druker up for any questions you may have. [applause]

[inaudible conversations] >> thank you for coming. the disease caused the mutation or did the mutation cause the disease? is that a model for other cancers, too? the way we look at other cancers? or does -- are they completely different kinds of diseases? >> you want to start with that one? that was a question when nothing was known. right? it's hard to imagine in a way a time when we did not think of genes as being involved in cancer at all, which was part of the story i wanted to tell. that -- to show the evolution of scientific thinking, but that is, as i understand it, from

this -- that is one of the major questions now, is when these mutations are found in a tumor, to understand, is it driving the cancer? is it a driver mutation? or not? and how to know and how to figure that out and how to find drugs to treat that. i would ask the current -- >> our current view of cancer is that every cancer will have a driving abnormality, meaning something is broken that is driving the growth of the cancer. but as jessica pointed out a lot of the cancer doesn't carry a lot of additional abnormalities that have nothing to do with it. called passengers. right now the termology is they're driving when you think of driving the cancer, and passengers just go along for the ride. we have to understand the differences in which the drivers are because those are the ones that can target a drug like

gleevec and see dramatic responses and changes the way we think about cancer and it treatment. >> it's a layperson question. you said that -- i thought you said that the chicken story was actually -- it was a virus that caused the mutation, so that's one question. the other one, the other thing you said is that when the chicken died, he took the tumor and injected it into another chicken. so you said cancer is contagious. but how else is it contagious if it doesn't -- how does the tumor get from one place to the other? here it was injected. kind of two questions. >> so, that was in animals and was a virus. okay? so -- it's the virus that is

contagious. viruses are contagious. the physical matter of a tumor is not. it is just matter, right? so, in people, cancer is for the most part not contagious, does not contagious cancer. there's human papillomavirus, we know, can lead to cervical cancer. 20% of cancers have a viral connection. that's the right -- >> between 20 and 30. worldwide, hepatitis, liver cancer. but, yes. 20% in the u.s. probably. >> okay. so, for the most part, it's a phenomenon of animal worlds and what he had -- what peyton rose had proven when he ground up the tumor and injected the purified extract into another chicken was that there was a virus in there.

that is what he was showing, and he was studying the virus and turn out the virus -- virus contain -- they're wonderful to work with in the lab because they contain four or five genes and they can over the years later take one out, was still causing cancer, and if they took one dean out and the virus did not trigger cancer, they knew that was the gene that was triggering the cancer. so it's a way to study how cancer occurs for many years. >> what is amazing about the experiment that peyton rose did, actually took the tumor, grounded it up and put it through a filter so no cells could get through. so no tumor cells just this extract with no cancer cells in it and injected it in another chicken and that chicken got cancer because it was a virus. the virus picked up a gene

inside a normal cell of a chicken and changed it around so it gave the cells a growth advantage and that became the temp template for understanding that genes can be stuck on, a green light to cause cell growth. so amazing that for 50 years nobody -- until 1910, 1911, and in 1950s we cultured the viruses in a petri dish. and people realized he was right. and after he made this discovery he won the nobel prize, and the oldest living nobel prize winner and it has to do with the fact you have to be alive to win the nobel prize and he was in his

80s, so he lived a life that set the groundwork for the modern era of cancer genetics. >> it was just a few years later that won the nobel prize for discovering the origin of cancer. the discovery that peyton rose, who he was being recognized for later, was awarded very soon after. the timing is amazing. questions? >> i can't wait to read the book. sort of reminds me of the book by rebecca -- the henrietta story about cancer, not only the science but the sociology of the story of cancer and medicine,

and i'm really interested in learning more about that. and i have a very good friend who is a cancer survivor, and has taken gleevic for the gist cancer she had and has been surviving very well with gleevic. i think this is a great story for what the repercussion on families. i'm a person that has lost someone to cancer, and my friend, who is a cancer survivor with glee iv c, she lost her husband to brain cancer, and cancer is like divorce, the effect it has on families. cancer can cause families to implode, and the beautiful thing is, is that my friend, who was a widow, raising these children, you know, her husband who died of cancer, you have to live, and so she did. she got her doctor to give her

gleevic for are her gist cancer even hoe she didn't have leukemia. so that is a permanenter and -- personal experience and it's wonderful these breakthroughs that come out at a grassroots thing. it's not leading by institutions but by individuals trying to, as you say, miraculous efforts to fund these efforts. so my question is -- i do have a question. are there many patients taking gleevic for other cancers besides leukemia, and specifically how many just cancers have been treated with gleevic? >> the numbers for gist, which is a gas the intestinal stromal tumor is 2,000 people per year and a quarter of them will be treated with glee iv c. 0 if you look at the numbers worldwide, quite a few on

treatment. gleevic is now approved for ten different cancers, and it gets at one of the critical issues that jessica was alluding to, and that is redefining these broken parts, what keeps that green light stuck on, and we're finding that sometimes what is causing the green light to get stuck on in leukemia is an intention until tumor or skin tumor or other cancers and can use the same drug in ten different cancers and that's part of the reason novartis was able to see a return on invery much, they can use this drug for not just one tumor but ten different cancers. >> an molecular level how does gleecic operate? >> as jessica noted, there are

these enzymes, and enzymes can be part of the on and off switches, and they make atp, kind of the energy exchange system in our body, like our body's money. if you want something to have, have to pay some money and the body uses atp. and the kinase bind atp and transfer to another protein and that tryingers cell -- triggers cell growth. so, get to that in a second. the way that gleevic works, it blocks atp so it can't trigger the signaling, can't turn anything on.

and atp and a dollar is a dow dollar and how do you have specificity. the result is -- there are 500 different kinases in our body and they all have slightly different structures and we now have the crystal structure, three-dimensional structures of hundreds of different kinases and they're all a little different. the reality is there's probably no one of those drugs that shut down one. they will shut down anywhere from two to 50, depending on what they look like. >> there's 300 an normal kinass or -- ...

probably somewhere in the range of 10-20%. >> i think you probably answered part of my question. my original question was how could you tell early on -- or how could people tell early on that they would be the big target and then how could you tell that inhibiting and plot to the end of what you said, is it a common pathway for cancer in general? could you comment on some of those things?

>> they are a very common pathway for cancer and they regulate cell growth and any time that regulates growth will be a target to get stuck on in the green light analogy. the way that we knew that this particular enzyme was the right target was present in every single page. and it basically defines the disease and what was discovered and she does a fabulous job of going back to the 70's and the 80's of all of the researchers who contributed to that identification that comes out of the philadelphia chromosome. when i came into the story i went into the laboratory and i said if you make some changes to make it completely inactive so it can't function as an enzyme what does that do when you put it into the cell and it does nothing. you put that into the cell and

they grow like wildfire you make a mutation that makes it an inactive protein that does nothing. so clearly the was the right target. >> i will add one thing left just some of the hench become history of this fascinating to me when people were first researching this before there was an understanding of the role in cancer, there were five to ten of them that were known. there was a man named sir philip cohen from england who told me all about the research. and he said you know, we knew nothing. these were interesting proteins that had other elements -- ailments. when the will be played in cancer a was like a lightbulb moment of of course it turns out that it's the perfect way for

cancer to happen. and with heavy app process that dr. druker described, you can think of cancer has been an incredibly efficient. as he put it to me it is a kind of sustainable energy model that cancer cells use in the body and of course that turned out to be correct. because there are so many that are involved in cancer. >> you said there's about 20% generated. what about environmental factors that are generated, and are there just cancers that start fueling spontaneously without any outside actors? >> it depends on what you consider to be environmental. the most common, smoking is 30% of cancer. how does it do that? the way that it does that is it

injures the cells in the lining and dna and damaged dna as we have been discussing the right place at the wrong time you have cancer. so you think about any environmental cause it is going to be things that damaged cells causing them to grow with things that damage the dna directly. the estimates ranging or 5% environmentally caused. it may be more or less than that that is the average life seen from a number of studies that have been done. but the reality is can i see cancer because i see it as a genetic disease meaning it is caused by changes in the happen.

so almost 1 trillion bits of information has to be replicated and there are going to be mistakes. and unfortunately as we get older they accumulate in the body and if you look at the number of people that get cancer it rises very steeply after age 50 and to me that is just a accumulation of mistakes over time. >> the philadelphia chromosome a spontaneous. it's never been connected to an environmental toxin. research has been done and still goes on because you never know when you will find. but it is a spontaneous mutation. as it was just described the dna replication has mistakes. those mistakes can arise and disappear without us even knowing. but sometimes -- about 5,000 people per year there is a mistake and it's spontaneous. it isn't passed on but it can't

be prevented or predicted. >> you mentioned the chicken cancer. i was curious about the link between cancer and animals and cancer in humans, like whether or not if you injected some chicken meat that had cancer that you could catch chicken cancer as a human. >> i mean i hope not. i don't think that is a real concern. but i suppose there could be a lie of by riss live virus. it is active in chickens and not every active will be in the people. >> to certainly recognize that as an animal virus and kill that i wouldn't be too worried about

injecting the virus from animals. then again as people look very carefully at cancer to look for viruses, again at sounds like with the papilloma virus but outside of that there aren't that many that we are seeing. >> is there any evidence of resistance to the treatment drugs and will this lead to the need for some kind of cocktail and different types of drugs that some have used in the aids virus? >> great question. so, yes. going back over the years it has worked for a number of patients, but there were some that didn't respond to the drug or stopped responding. for example, and there was the

late stage patients in what is called the last crisis. there was a patient i write about in the buck who was brought in in a wheelchair. she had chosen her burial plot. she was -- she really thought this was the end for her and her husband brought her into the clinical trials, brian druker and started her and she is still alive. but there were patients who would after a couple of weeks get up and walk out of the hospital, get up from their wheelchair and dance out of the hospital and have these recurrences just as quickly they would be back in the wheelchair. there was a man who was very driven to understand why that was happening. he was one of the investigators who wanted to understand why this was happening. and eventually that research led to the understanding that sometimes there could be other

mutations that would change the shape of it a little bit more. and so if you picture like i give the analogy in the dhaka covering with my left hand. but if you move the face a little bit you change the shape of something it's not going to fix. if the shape of the lock changes a little bit the key won't work anymore. and so, there were efforts to find those that would fit but that had a slightly different shape and that led to second and third generation. and anyway most of the mutations now there are drugs to address those. yes. >> you take a disease where the first company thought there was no market and now there are five

drugs for this disease and the resistance it runs about ten to 15%. and in ten years it is still only about 15 to 20%. so most people -- some have had to move on to the second-generation drugs. learning other answers the response tends to be relatively short. we do need to think about understanding the resistance much like we do for hiv and maybe it is a double triple combination will result in the very ability and good toxicity profiles for the patient is. >> one or two more. i guess this question is for dr. druker. did you create a cure for the cancer? >> it's funny my wife is also a

writer to be the doctors don't like to use cure because to me it has a certain definition. but if you talk to most people and say this insolent your diabetes most people say yes. it to a doctor, it treats diabetes. but you have to take the medication in order to be cured or treated. but because the public kind of looks at this as a treatment and it puts it into remission and you are fine and you can stay on it forever that is close enough. >> that was one of the reasons why the financial worry turned out to not be important, right? because the drug is taken once a day for the rest of the person's life. so, for that reason, there was

no reason to be concerned financially. any more questions? >> i want to address the idea and you talked about how difficult it was to get the fda approval yet i am hearing now that there are certain cancer treatments that are being fast tracked for cancer treatments. why is it they are doing that now? what is necessary to get those fast tracked? >> so, i will respond. i think that we should both respond because there is so much to say. first, the fda did not block this drug, they were not standing in the way of this being made at all. in fact, there was a moment where the drug company was saying we need more animal

studies, more toxicology data. and he went to someone secretly and asked, you know, isn't there enough data and they were like yeah, you have plenty. and when the drug finally -- wendi the. once it got into the clinical trials it was two and a half years. but the entire year development took 18 years. normal drug development, this is like eight to ten years. so, what took a long time was in the fda. sometimes it can be. but in this case, no it was the fastest approval ever. fast track is one of a few different designations that an experimental compound can get when it is known to be addressing a disease where there are no other satisfactory treatments available and the compound looks particularly

promising there are mechanisms in place to help speed up the drug through the process. basically what all of these designations amount to is more time that if someone needs to work later hours they will work later hours. that is really what it boils down to is more attention. they will meet with the drug company in advance and say this is what we need from you. so everything is laid out as soon as possible. and now there are more mechanisms trying to be put in place. the bureaucracy is just a killer. for example, it is problematic to use the two experimental drugs in clinical trial because he would think there's all these experimental drugs. if there's going to be cocktails why can't we test two of them at once and move the whole thing along? but you cannot use these in a

trial most often because when the side effect occurs you will know which one it came from and then there's all kind of other red tape involved in that. so there are things that stand in the way but there's definitely an attempt to improve the situation like the zero clinical trials you can test on fewer patient. like this was tested on hundreds of patients the data came from hundreds of patients. it's all about the, some it's all the same disease. so it's given a kind of conditional approval everyone would have gotten a lot faster. so things like that could be in the works but it's difficult to get them working.

>> they've come up with a new designation called a breakthrough visit nation status which fast tracks drugs. it puts the company is in contact with the data and help them shepherd through very quickly but they are for these targeting drugs meaning it is about a thousand patients about the response we got on the first 100 were the same in the last. so the reality is that we could have taken the first 100 had a breakthrough designations that this we could have had this in a year, not two and a half years. so things are changing and it actually is willing to learn and listen and moved when there is a

medical disease. >> one last question and then we will wrap it up. >> in the future are there going to be incredible vaccines against the cancers you could take and avoid the possibility of getting it at your old age? [inaudible] the vaccine for human papilloma virus that presents 70% of cervical cancer pity there's also been recent incredible success with a couple of immune stimulatory drugs that detect cancer and there is in particular. we took the same approach that we did with infectious disease which was antibiotics which i

see is targeted devotee, vaccinations and we have seen the system to think about the early diagnosis and prevention. and if we take that approach in this century i'm extremely optimistic it will make a huge impact on cancer in our lifetime >> i will add briefly i said earlier that one of the reasons why i wanted to write this book is like the origin story for the current times. it's like it's the foothills of the mountain that researchers are now claiming where cancer is concerned. and definitely that is the hope. we have all been touched by cancer in some way. there's i think 14 million people in the united states who now have a history of cancer in their lives. and when i asked brian will there be something for every cancer because who doesn't want that?

and his response to me at least a year ago was that the current division, the short term vision was the tumor genome sequencing. so not personalized, not like the 23 find out everything about your dna. but when somebody has a cancer to look at the genetics of that cancer and try to screen it for the mutations in the rapidly scream compound that could work against those. and that is like the 20 year vision. alongside many other efforts going on. >> thank you so much. thanks for the great questions. [applause]

new i am the beneficiary. i had a daily nocturnal pain. if i didn't know better, i would think that i had cancer of the bone. i saw the best surgeon and i got a wonderful procedure. a week ago i played nine holes of golf. that is how good it is. i would challenge anyone. they need the right medications.

you probably need a good orthopedic surgeon. so, with the madison it does amazing things and we shouldn't forget that i had occasion that required 100 units of blood and they ran the boston marathon. the if major role in preventive medicine. how do we prevent obesity, how do we prevent and can we cure these. there is in line a certain limit. [laughter] >> i have actually experienced. i had knee surgery and out of the blue suddenly it was swollen

it was pretty depressing on the spring day in boston and then i need a friend and she said you mentioned that you got relief from your back pain. it was really hurting in this land. i got acupuncture and then she got out of the car in the parking lot of the country club and kicked her foot into the air i called them early in the morning. i went to see her and she did the acupuncture and i got up. you can compare one to the other. suddenly it is gone. i don't believe it. i can't understand how it happened. my wife wasn't there to beat she

was going to come home to hours later. she was doing some shopping. i went to the country club and i played nine holes of golf. and i benefited from acupuncture and things of the sort. >> i benefited from what i practiced and i don't make believe could take any medication's never had surgery, never been hospitalized with it but i agree with much of what he said but want to answer your question because she asked me a specific question about the medicine practiced. he comes from harvard medical school which is the gold standard and many other places like that. but there are some statistics. [laughter] here are some specifics. between the disease has been

dubbed a result of medical treatment. it wasn't a bit of a difference in the natural history of the disease except the medicine, some side-effects and money. >> [inaudible] it would cause death [inaudible] [laughter] now also the most common is the bypass [inaudible] it doesn't prolong life and more than 2% of people but it's the most common procedure. the second most common procedure is angioplasty, doesn't prolong

life for stabilize more than 3% of people. these all are alarming statistics that have been done everywhere. back surgery, 98% is useless. hysterectomy, 95% is useless. so we are talking about huge amounts of money spent on the procedures. my father would make a diagnosis, neurological diagnosis. today if you have a headache and go to the emergency room if you don't walk out with a cat scan or mri, and you are lucky. as we have a crisis. what we call health reform isn't health reform. none of the expenditures end of life care nobody is allowed to die in the house.

i said i'm not going to die in the hospital and i'm not going to have any of these resuscitated if procedures. i've been in community hospitals where the same standards don't apply and i see doctors directing something called a little boy not minor but aberration and electrolytes and the patient would die but to keep correcting it even though. a lot of what we call the prolonging of survival is of suffering. for the patient, the relative, the only people that make money for the medical providers. i even brought it up to our president. but we have a system to the we have a system, and again, nothing to do with the gold

standard practices. we have a system there for every congressman with a 28 lobbies in washington. the only business with the medical industrial complex lobbyist for the military industrial. so you know, where do we think our country makes money? is it the supply to afghanistan or india? we have huge problems when the incentives for treatment become money and it becomes then a corrupt influence how do you think a can of their past makes money? every chemotherapy treatment that they get to the am i singing you shouldn't have it? i am not saying that. i ask everyone here to be a

difficult patient. question number doctor. ago to google and get the information and did you will know more than the average medical provider. [applause] up next book tv sat down with a journalist and author simon jenkins in london to talk about british politics and history, journalism and architecture. mr. simon jenkins is the author of many books including battle for the fault land and a short history of england. >> now joining us from london on book tv is simon jenkins. here is a little bit about our