facebook.com/booktv. >> up next, jessica wapner, author of "the philadelphia chrome sewn," talks about the discovery of a mutant chrome sewn by a scientist in 1959 and the eventual realization that the mutation is the sole cause of a certain kind of lieu chemoya. this led to the first-ever successful treatment of cancer at the genetic level and opened up a new field of cancer research. this event, hosted by powell's city of books in portland, oregon, is just over an hour. ..

it is great to see everybody here. so i am going to read you an excerpt from the book, just from the very beginning so i am not giving anything away and talk about why i wrote the book. why i think this story matters. why i felt it needed to be written down. it is important because of its eternal the important qualities and also why now? why this story at this time? and have time for a q&a.

i will begin with the excerpt from the preludin which is entitled down to the bone, february of 2012. gary eikner said in a chair back against all. across the room his nurse was half hidden by computer. she scrolled through his medical charge. on a monitor he couldn't see, typing his responses to her questions. he answered and smiled as if he were just fine, as low that would somehow make it so. he kept his field silently wondering what the next hour would reveal about the disease that had so suddenly overtaken his life. fear permeated his every thought. the nurse ran through the litany of side effects he might be

experiencing from the leukemia medication he had begun to take. any chest pains? heart problems? any swelling in your ankl any problems with nausea? eichner's know was tempered by his description of what he'd happened when he took the drug on an empty stomach. massive pain in the stomach he told the nurse, like the worst thing you ever had. the nurse knew that eichner had no idea the worst things someone with his type of leukemia could have. few patients with his disease today will ever know that kind of pain but if the nearest was thinking anything of the sort she kept it to herself. after all her patient was about to have a large hollow needle inserted into his bone so his doctor could extract a sample of marrow. having witnessed countless such procedures during the 12 years she had been a nurse to patients

taking the drug she knew how much was riding on this biopsy and she knew that eichner, age 43 was aware his life was at stake. if anyone could set him at ease it was his doctor, brian druker. all i care about is you are making some progress, druker told his patient who had come to portland, oregon for a bone marrow biopsy. the procedure would reveal whether the medicine, a bill he had been taking daily for six months was tackling the leukemias that had invaded his body. eichner had chronic myeloid leukemia, 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. eichner nodded his understanding his jittery foot the only sign of his nervousness.

for eichner those numbers were part of the new language he had learned since his diagnosis in summer of 2011. as with so many cancer diagnoses the education began unexpectedly. after a day or so of sharp excruciating kidney bean, eichner, single-parent of a teenage boy, drove himself to the emergency room at his local hospital in olympia, washington, where he had been living. his sister-in-law, a trauma flight nurse told him she thought he had kidney stones. so he was expected to be admitted for a standard albeit painful procedure. when several doctors walked into his hospital room together he knew something wasn't right. you don't have kidney stones, they told him, you have got what we believe is leukemia. a blood test soon revealed that

eichner in otherwise excellent health had an excess number of white blood cells, confirmed that much. the doctors explained the stabbing pain he thought came from his kidneys probably was from his spleen, and large by the high concentration of leukemia cells within. although the slow-moving nature of the disease meant he wasn't in immediate danger there wasn't any time to lose. for the best chance at long-term survival he needed to start treatment right away. as eichner was informed danger could eventually come. if the treatments didn't work, within five years his bone marrow, white blood cells that failed to mature, overly abundant and thoroughly useless, his blood, once free-flowing, would turn into this this sludge. the supply of fire rich red blood cells that carry oxygen

around the body would steadily plummet leaving him fatigued and anemic, the decrease in the number of platelets would render his blood unable to clive. as the disease progressed the miniscule capillaries leading to his eyes and brain would clogged, his spleen would become profoundly and large. as his body began shutting down he would bleed in his brain, in his intestines and out of every orifice. two days later eichner was having his first bone marrow biopsy performed by a nurse who spoke broken english and had to climb on top of eichner to hammer in the four inch needle to break through his bones which had become hardened and inflamed from the profusion of white blood cells. finally she managed to extract an ounce of marrow. the spongy matter in the center of the bones were new blood cells are made. in the genetics laboratory

fluorescent dye applied to the coil strand of dna inside eichner's blood cells revealed the telltale sign of c m 0, genetic mutation known as the philadelphia chromosome, and abnormal chromosomes regarded the defining feature of this fatal, spontaneously arising cancer, and discovered more than 50 years ago. twenty out of 20 cells in a sample of his marrow contained this genetic error. a family friend with the same type of cancer told eichner to call dr. brian druker right away, don't do anything until you see him. three days later, he got a call from druker who mysteriously eichner didn't know how it got in his phone number. during the next 20 minutes, druker talked him down from his

panic assuring him that being in the ear of the stages of the disease eichner could wait a week or two to oregon health and science university where he had been treating and researching leukemia since 1993. he gave eichner his professional blessing to drink beer. it was august and eichner had been getting ready for summer grew fast, his brother's idea for getting his mind off of leukemia when the phone rang. ten days later, eichner was on his way to portland. within three weeks of his diagnosis he was swallowing his first tablet of medication which druker was instrumental in developing. a drug aimed at tackling the cancer at its roots. i won't leave you in suspense. this is the beginning of the. gary eichner is still alive.

was supposed to be here. i was hoping he would walk in right after the excerpt. six months after he began taking the drug that i write about in this book, his test came back 0 out of 20. you remember i said when he was diagnosed he was 20 out of 20 meaning in a sample of cells taken from his bone marrow 20 out of 20 contained a genetic mutation called the philadelphia chromosomes so six months later after taking this drug it was 0 out of 20. i would like to start with that except because i think it shows so much about why this story is important and why i loved it so much because of the impact scientific progress has on our lives and this unstoppable drive that we have to make tomorrow

better than yesterday and the length people will go to to ensure that that progress happens. when i first began researching this story, i didn't know it would be like this. i was working at a medical journal in 2000, then i would hear this word "the philadelphia chomosome," when data was starting to emerge from some studies and i didn't know what it was but the name is very captivating. it is a great name for a genetic mutation, "the philadelphia chomosome". years later i became a free-lance writer, wanted to dig in a little more, to understand what was it, maybe there was the magazine article, i started talking to some people, including brian druker and other people i knew by that point and my research began with the question of why is it called "the philadelphia chomosome"? as you might have guessed, is called that named after the city

where it was discovered. in 1959 two scientists, were researching sells looking through a microscope resurging different cells. peter noel stumbled across this method for expanding sells more even they had been expanded before end because he was in a hurry he was very dangerous to cure cancer actually, young and ambitious and thought he could do it in the summer so rinsed under tab water instead of the special laboratory water. the cells ballooned out and suddenly he could see chromosomes of a little bit more than people had been able to see them until that point. this is in 1959 compared to what we have today it was still quite course but it was new, something

different. peter knoll was not interested in chromosomes. at that point there was very little knowledge, no knowledge about the connection between genetics and cancer. no one was looking for the cause of cancer in our genes. he figured someone would be interested in this and as it turned out, that someone was david underford, in philadelphia, he was this very old school scientists, loved to look through the microscope day after day, he was not trying to cure cancer. he was not really trying to do anything but what he loved which was to observe so he started working with peter noel and looking at chromosomes through the microscope and one day was looking at some cells from a patient with cmo and noticed one

of the chromosomes was a bit too short. he was one of a handful of people probably in the country if not the world who could have spotted this at that time and what he saw is on the cover of the book. but it was this. chromosome 22, the 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 with the cancer causing mutation, was the mutation causing the cancer? so that was my first entry point into this story. as i began researching the science, understanding how this became unraveled, how but

philadelphia chromosome did turn out to be connected to cmo. the twist and turns of the science i thought it needs to be written down and i will give you an example. we have in ourselves protein, an enzyme that sets things in motion. and one type triggers the production of white blood cells and it happens in a stock and start way, always making blood cells, sometimes giving the signal and sometimes not so red light and green light so that is the normal kind but with the philadelphia chromosome mutation, triggers the production of white blood cells is mutated and in that mutated state it goes haywire and always

triggering production of white blood cells, green light, constant. i wanted to understand, how is it known that it was involved with cancer? i spoke with ray erickson who was the first scientists to uncover the connection, to find the involvement in cancer. how did you get there? i was researching a gene, looking for the protein product, why were you researching stock? that was a gene that was involved in chicken cancer. why were you researching chicken cancer? he used to get made fun of for resurging chicken cancer in the 1970s and the story went like

this. this was the gene involved in a virus that causes cancer in chickens and when he went to find out how did it cause cancer in chickens was when he understood the role of kenny's this and where the gene had first been found was all the way back to 1910. this is just to give you an example of the twists and turns, we just never know where science will lead or where it has come from that matter so this is a true story. in 1910 there was a scientist who was researching at rockefeller institute now called rockefeller university in manhattan and he had gone there in 1909 and been researching for a year and one day this woman shows up in his lab carrying a chicken with the tumor sticking

out of its belly. a true story. she walks up to his lab, looks at him and says can you operate? can you operate? he says sure, why not? so rockefeller institute has the first ever concerned jury and he removed the tumor but the men did not survive the there were remnants of the cancer in its body and it died but now a in had this tumor and figured i have got to research this.peyto had this tumor and figured i have got to research this. i won't waste this. so he injected into a chicken and it gets the same cancer as the first one. contagious. cancer is contagious.

what was important about this story is not so much that peyton discovered contagious chicken cancer which is very fascinating but that research eventually led through the research, led to the understanding of the genetic underpinnings of cancer, the cancer can begin in our own machines because it turns out the culprit gene in the chicken virus had come from the chicken itself. and that was what led people to understand it can happen in us. if you think about it, a preposterous notion because how would, why would our healthy dna undergo a mutation and in that mutated state trigger something that kills us? i love that story. to think that our current

understanding of cancer goes back to this farmer who brought her chicken to a laboratory to undergo surgery. first of all it would never happen today. the paperwork alone, she would just say i don't eat chicken. so the science was very interesting to me. but then it was when i started to understand what happened next that i bought this has to be a book. this is more than an interesting story. in the 1980s when the picture became clear about how the philadelphia chromosome leads to cmo which i just described to you there were people who started to think could we make a drug that targets that? could we make a drug that blocks

that eyewear -- stops the cancer at its root cause? this drug had never been attempted before. it had never even been thought about before. one of the people asking that question was brian druker. he worked with people at the time in the pharmaceutical company at the time, in switzerland, who were also asking could we make a drug to block the cancer at its root cause and after working at the chemistry for a couple of years which is a fascinating story in its own right, i am turning into a chemistry lover completely. they had a few compounds and they sent them to brian druker who was in portland and they didn't tell him which one was the one they thought was going to work so he tested them in the

lab and right away could see one of them was killing the cells so he did the same thing, given to his student, didn't tell them which were working, which one was the one and the same thing happened so you would think having seen that result in a laboratory, the pharmaceutical company would move rapidly into the next step. that would be the normal thing having seen such promise in the lab the next step would be animal studies and if proven safe in animals studies, human trials. but what happened after those initial tests were done was that everything ground to a halt. everything ground to a halt. i wanted to know why. i wanted to understand what happened. because this compound came so

close to not being made, i wanted to know why was it, how could it be that it was almost shelved. and talk about a couple of what we learned. had never been attempted before. it was risky. if the drug ended up blocking -- as one of the investigators put it to me, that was going to be one sick patient. it was a risk. you don't know what is going to happen when you give it to people. disasters like what happens still hang over the pharmaceutical industry. this was a drug that was

supposed to help women cope with pregnancy and ended up deforming their babies. weather that or numerous other instances that happened, nobody wanted an event white that to occur. zimmerman, the chemist who made the compound that eventually would be called lee su but back, you can look at this drug and say wwhy did take so long? why did you risk it? how did you do that which i thought was a fair point. and there were problems. there was a point where the drug for the drug was tested on animals after some delays end it was tested on mice and dogs and

rabbits and monkeys and hamsters and some other cell lines and there were problems at one point in dogs who were experiencing liver toxicity and brian druker got the message there were these toxicity problems and they were not sure they were moving forward. at the drug company, leading the drug development program at the drug company, hearing from a toxicologist who was conducting the animal studies telling him that over my dead body will this compound going to man. but brian druker is saying okay, there is liver toxicity in dogs, but you have to give this dog a chance. you are giving 600 milligram doses of the drug. a clinical child starts at 25

milligrams. we know the signs of liver toxicity. we are doctors. that is what we do in the critical trial that is the best health care a person can get in the clinical trial. if there is a problem happening we will see it and stop the drug. won't keep giving it until they have extreme liver toxicity. given the drug a chance. that wasn't the only problem. the other issue was the money. 6,000 people per year in the united states, up to 75,000 people worldwide, and diagnosed in 230,000 people. in the united states. and all types of cancer,

1.6 million people in the united states. 1,605,000. the drug company could not see how they were going to recoup on the investment. the patient population was a market as it was called was too small and they were looking at fact through the eyes of the business model in chemotherapy which was given for short amounts of time. they couldn't see how they will recoup on its investment. so eventually the drug went into a phase one clinical trial starting in 1998 and the results were stunning. in a clinical trial that is only supposed to be testing for safety patients were having incredible responses.

100% of patients had not he but the logic response with blood counts returning to normal. the normal range of white blood cells is around 10,000, up to 10,000, patients could coming to the doctor with count of to 100,000 and after a few months on this drug back in the normal range. even after the phase one study when those results are coming in, there were still delays when it would move from phase 1 to phase 2 because all the doctors conducting the study are saying we have to get this drug to everybody. every cmo patient that wants this drug should have and have it now. there were still delays. and this is one of my favorite

moments in the book. there was a patient named susan mcnamara from toronto and what was happening when this was going gone, perfectly timed with the rise -- couldn't have been better. cmo patients to find support and others going through the same thing you are going through. you won't find many people in your town and you're sitting with this disease but online, a whole community to be found of people going through what you were going through being treated with interferon which is a primary drug given to patients with cmo which is a very harsh drug, very harsh drug. or into a bond -- bone marrow transplant which is the -- still

the only technical queue or for cmo but if you survive it, about a 50% chance and if you are eligible for it and can live with the side effects which lasted lifetime. so susan mcnamara was very sick and living between her bed and her computer two feet away and would go on to the cmo chat room and reading reports from people in the clinical trials posting about how great they felt when blood counts were back to normal and having incredible response to the drug. so druker asks to be on the study and he says i will put you on the waiting list but is waiting list was 100 patients long as and when you get a new

drug he got permission, who was the sickest. and to the waiting list, i don't even know if the drug that will be made. and maybe you could do something. and i just felt there was no way there was a drug in this world, no way that we were going to get, wrote a petition signed by hundreds of patients within weeks, send it to know vargas, and the phase 2 child opened -- phase 2 trial opened. that scratches the surface.

and frustrating moments in this story. i just felt this needs to be told because in part because this is an origin story for this moment in cancer research where we are learning so much more about the link between genetics and cancer, it pulls back the curtain on how medicines are made in the science that goes on and the politics that can go on and the knowledge so that when we as health care consumers think about the world that we live in, we know the facts of what goes on but also, not only the story of this miracle drug but also the story of the miraculous links people will go

to to ensure their vision, their belief gets a chance in this world. that concludes the top portion for now. i will invite brian druker up for any questions you might have or sits over here and be happy to answer your questions. [applause] okay. >> thank you for coming, jessica. any questions, what caused the mutation or did the nutation cause the disease. is data model for other cancers too, the way we look at other

cancers? are they completely different kinds of diseases? >> would you like to start with that? that was the question when nothing was known. it is hard to imagine in a way a time when we did not think of genes as being involved in cancer at all which is part of the story i wanted to tell, to show the evolution of scientific thinking. but that is as i understand it, that is one of the major questions now, when these mutations are found in a tumor, to understand is hit driving the cancer? is jenna driver mutation or not? how to know, how to figure that out, how to find drugs to treat

that? >> current view of cancer is every cancer will have a driving abnormality, something that is driving the growth of cancer, just pointed out a lot of the cancers kerri along a lot of additional abnormalities that have nothing to do with it. the terminology, drivers, things that driving the growth of cancer, go along for the ride the. we have to understand the differences what the drivers are because they target this drug and see remarkable responses that really change the way we think about cancer and its treatment. >> note layperson question, you said -- i thought you said that the chicken story, a virus that caused the mutation. that is one question and the

other thing you said is when the chicken diet it took the tumor and injected it into another chicken, that cancer is contagious. how else is it contagious? how does the tumor get from one place to another? here it was injected. two questions. >> that was a virus. it is the virus that is contagious. viruses are contagious. the physical matter of the tumor is not. it is just a matter. in people, cancer is for the most part not contagious. there is not contagious cancer. we know certain viruses lead to cervical cancer, 20% of cancers

have a vital connection. >> worldwide, hepatitis with liver cancer, but yes. 20% in the u.s. probably. >> so for the most part it is a phenomenon of the animal world and so what he had, what peyton had proven when he ground up that tumor and injected the purified extract into another chicken was there was a virus in their. that is what he was showing and he was studying the virus and it turned out the virus, viruses are wonderful to work within the lab because they contained four or five jeans and over the years later, take them out, still causing cancer, and if they took one gene out and the virus did not trigger cancer than they knew that was the gene that was

triggering the cancer. it is a way to study how cancer occurs for many years. >> what is amazing about the experiment was to expand a little bit, actually took the tumor, ground it up and put it through a filter. no tumor cells, just this extract with no cancer cells injected in another chicken, it was a virus. it picked up a gene. and change it around for a growth advantage. this is the template for understanding jeans if changed around canby's become stuck on. what was so amazing was for 50

years no one believed peyton. probably got some tumor cells and this is what happened but in the 1950s when you culture these things in a petrie dish, in 1966. and the oldest living nobel prize winner, allowed to win a nobel prize, live a very long warfare productive life in the modern era of cancer genetics. >> it was just a few years later they won the nobel prize for uncovering the cellular origin of cancer. this discovery that his work led to that he was being recognized for 55 years later was awarded very soon after.

the timings are amazing. questions? >> can't wait to see the book. this reminds me of the book by rebecca salute, the story about cancer, not only the science and personal patient history but the sociology of the story of cancer and medicine. i am interested in learning more about that and i have a very good friend who is a cancer survivor and is taking bluevest for the gist cancer that she has so she is surviving very well with that. i just wanted to say that this is the great story for what the

repercussions on family, because i am a person who has lost someone to cancer and my friend who is a cancer survivor lost her husband to brain cancer and sometimes i think of cancer as sort of like the bourse. the effect that it has on family. cancer can cause families to implode. the beautiful saying is my friend who is a widow raising these children, you have to live. so she did. she got her doctor to give her leeback for her cancer even though she didn't have leukemia. that was a great story from personal experience in san francisco and it is wonderful these breakthroughs that come at grassroots, it is not systemic or -- as you say these miraculous --

>> my question was are there many patients taking it for other cancers, specifically how many just cancers have been treated with the leeback? >> the numbers for gist which is gastrointestinal strong tumor is 2,000 people per year and a quarter will be treated with it so if you look at the numbers worldwide it is quite a few on treatment. it is now approved for ten different cancers and one of the critical issues jessica was alluding to as lee d. find these broken parts which keeps the green light stuck on, we are finding that sometimes what is causing a vote green light to get stuck on is intestinal tumor

or skin tumor or other cancers and use the same drug in ten different cancers and that is why no vargas is able to see a return on investment, not just one tumor but ten different cancers. >> on a molecular level, how does it operate on a molecular level? >> jessica noted these enzymes, off and on switches turn things on and they turn things off and these enzymes find what is called a tp, remember your high school biochemistry, atp is the energy exchange system in our bodies like orebody's money,

body uses a tp. what these do is they find a tp and transferred to another protein and that triggers cells. away it works is it binds into this, so it can trigger the signaling so it can't turn anything on. you might say a tp sounds like the dollar is a dollar and how do you have any specificity. the reality is all these -- there are 500 different kinds in the body and they all have slightly different structures and we now have a crystal structure, 3-dimensional structure of hundreds of different things and they are all a little bit different but the reality is there's no one of these drugs that shuts down

once. they should -- they go from 2 to 50 depending on what they look like. >> 300 abnormal ones? >> there are 500 in the body and probably 300 of them shown to be active in cancer one way or another and one of the most commonly what we call drug to target in the drug industry because they are so commonly mutated in cancer drug companies know they can make these drugs and there has been a successful paradigm. >> of all the personal things, how many have viral triggers? do they have all of them? >> actually very few, in the range of 10% to 20% will have some viral triggers.

>> you probably answered part of my question and my original question was how could you tell her lee on or how did people tell early on that -- this would be the big target? how could you tell that inhibiting the cottage would be specific and to go to what you said, is it a different kind of path way for cancer in general? could you comment on those things? >> it is a very common pathway for cancer and regulate cell growth and anything that regulate cell growth will be a target to get stuck on in the green light analogy. away that we knew this particular enzyme was the right targets goes back to the chromosomes. it is present in every single patient that basically defines

the dizzy ease and when it was discovered, jessica does a fabulous story going back to the 70s and 80s of all the researchers who contributed to identification of this chromosome, and going to vote library, making change to make it completely inactive so it can't function as an enzyme. the cells grow like wild party, and tumors, make a mutation that takes an inactive protein that does nothing? that was the right target. >> from the histories that was so interesting, when first researching before there was an understanding of their role in

cancer, 5 to 10 were known, sir philip, and from england told me all about the research, we knew nothing, and rolls in other ailments, and the role they played when cancer was recovered, a light moment, was not the way for cancer to happen with the atp process, you can think of cancer as being incredibly the efficient, there is a sustainable energy model, and that's turned out to be correct, so many are involved in

cancer. >> you say there is 20% viral generated and what about environmental factors generated and are there cancers that started spontaneously without outside actors? >> depends on what you consider environmental, but to attract the most common, smoking, 30% of all cancers and how does it do that? the way that it does is it injures cells in the lung lining causing them to grow and any time you grow you pick up some mistakes. in addition there are chemicals in cigarette smoke that damage dna and as we have been discussing, if the right place at the wrong time, you got cancer. so anything, think about any environmental cause, things damage cells causing them to grow, things that damage dna

directly. the estimates range anywhere around 5% will be environmentally caused. it may be more than that or less than that but that is what i have seen from a number of studies. if we are going to approach, the other reality is i see cancer as a genetic disease. it is caused by changes in jeans and any time our cells divide, they make mistakes. it happens. almost 1 trillion bits of information have to be replicated faithfully and there will be mistakes. as we get older these mistakes accumulate and if you look at the number of people who get cancer it rises after age 50 and to me it is an accumulation over time. >> the philadelphia chromosome is spontaneous. it was never connected to an

environmental toxin. research has been done and it still goes on because you never know what you will find but it is a spontaneous mutation has just described. dna replication has mistakes. those mistakes can arise and disappear without us even knowing but sometimes and in this case and 5,000 people per year there is some mistakes that occur is that leads to cancer and it is spontaneous, it is not passed on to one's children but it can't be prevented, it can't be predicted. >> you mentioned the chicken cancer. i was just curious about the link between cancers and animals and cancers in humans, like whether or not you injected some chicken meat that had cancer that you can catch chicken cancer as a human.

>> i hope not. i don't think that is a real concern but i suppose there could be a live virus, but this virus that hayden research is active in chickens. >> our immune systems certainly recognize that as an animal virus and kill it. i wouldn't be too worried about ingesting viruses from animals. again, people look very carefully at cancers to look for viruses. it is seen in some way as cervical cancer and head and neck cancer but inside of that there are not many viruses in cancer that we are seeing. >> is there any evidence of

evolution of resistance to the treatment drugs? will this may be lead to a cocktail, different types of drugs that are similar to use in the aids virus? >> great question. over the years, worked for a majority of patients but there were some that didn't respond to the drug, at a late stage patients and blast crisis, a patient named madonna who i write about in the book, was brought in in a wheelchair, and this was the end and her husband brought her into a clinical trial with brian druker and started her, she is still alive.

there were patients who after a couple weeks get up and walked out of the hospital and dancing out of the hospital and have these recurrences just as quickly back in the wheelchair and there was a man named charles lawyer who was very driven to understand why that was happening.awyer who was ver driven to understand why that was happeninsawyer 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 will lead to understanding there could be other mutations that would change the shape of a little bit more so if you picture i give the analogy in the book of my gloved hand suffocating a face. but if you move the face a little bit you change the shape of something it won't fit or lock the key, the shape of the lock changes a little bit the

key won't work anymore. so there were efforts to find drugs that would fit, a slightly different shape and that led to second and third generation versions of the drug. and a fourth generation. most of the mutations now, there are drugs to address those. >> they are actually, you are taking a disease where the first drug company thought there wasn't a market and there are five drugs for this disease and resistance at five years runs 10% to 15% and in ten years it is only 15% to 20% so most people are find but some patients had to move on to second-generation drugs or learn in other advanced cancers the reaction to these targeted agents is short. we need to talk about

understanding resistance and designing cocktails and drugs as we do for hiv and there is a double triple conversation that will result in higher response rates and good variability and good toxicity profiles that will be tolerable for our patients. >> one or two more. i guess this question is for dr. druker. you created a cure for cancer. >> my wife is also a writer and doctors don't use the queue or. the cure has a specific definition but if you talk to most people, the insulin cure diabetes most say it cures diabetes. insulin treat diabetes but you have to take the medication to be cured or treated but because the public looks at this as a

treatment and puts the disease into remission and you are fine and can stay on it forever that is as close to a cure as we need to call it and if people call it a cure won't argue the semantics of it. >> i will add that that was one of the reasons why the financial worries turned out to not be important because the drug is taken once a day for the rest of a person's life and for that reason there was no reason to be concerned financial lely . any more questions? >> reporter: you talked about. any more questions? >> reporter: you talked about the problems getting it approved and there are certain cancer treatments that are being fast

tracked for cancer treatments. why are they doing that? what is the need? what is necessary to get those drugs fast-track? >> i will respond. the fda was not standing in the way. there was a moment when the drug company was saying we need more animals studies, more toxicology data and brian west, someone at the fda secretly asked isn't fair enough toxicology data here and they were like yes, you got plenty. when the drugs, when the data did go to the fda it was the fastest approval ever. once the drug got into clinical trials it was 2.5 years but the entire development of the drug

took 18 years. normal drug development process is 8 to 10 years. what took a long time is not the fda. sometimes it can be but in this case no. it was the fastest approval ever. fast-track is one of the few designations as experimental compounds can get. when it is known to be addressing a disease where there are no other satisfactory treatments available lands where the compound looks particularly promising there are mechanisms in place to feed the drugs through the process and basically what all these designations amount to is more face time with the fda. if someone needs to work later hours they will work later hours. that is really what it boils down to, more attention, the fda will meet with the drug company and say this is what we need from you so everything is laid

out as soon as possible. .. >> involved in that. so there are things that stand in the way, but there's definitely attempts to improve the situation. like phase sear -- zero clinical trials where you could test the drug on fewer patients. like this drug was tested on, i mean, hundreds of patients, right, that the data that was