change these. [laughter] >> thank you very much. this has been wonderful. chip, thank you for this and hugh davis and john summers it has been wonderful. thank you very much. we will see you in the lobby [applause] . .

>> it's wonderful to be back. i'm glad it's not february this time, around just great to see everybody here. so, i am going to read you an excerpt from the 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 this story matters, why i felt it needed to be written down.

i think it's important because of its eternally important qualities, and also why now, why this story at this time. then we will have time for a q & a as you heard with dr. druker. ok. so i will begin with the excerpt from the prelude, which is entitled, down to the bone, february 2012. gary eikener sat in a chair backed up against a wall. across the room, his nurse was half hidden by a computer. she scrolled through his medical chart on monitor he couldn't see, typing his responses to her questions. he answered and smiled as if he were just fine as though that would somehow make it so. he kept his worry concealed,

silently wondering what the next hour would reveal about the disease that had so suddenly overtaken his life. it permeated his thoughts. the nurse ran through the litany of side effects he might be experience from the leukemia medication he had recently begun to take. any chest pains she asked, heart problems? swelling in your ankles? his no was tempered only by his description of what happened when he took the drug on an empty stomach. it's massive cramping in the stomach. it's just like the worse thing you ever had. the nurse knew nothing of the worst thing he could have. few patients with his disease will know that kind

of pain, but if the nurse wag 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 that 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 a drug, she knew how much was riding on this biopsy, and she knew that eichner was well aware his life was at stake f. anyone could set him at ease about that, it was his doctor, brian druker. all i care about is that you're making some progress, druker told his patient, who had come to drukeres chrin nick portland, oregon for a bone marrow biopsy. the procedure would reveal whether the medicine, a pill he had been taking daily for six months, was tackling the leukemia that had invaded his body. eichner had chronic myeloid

leukemia, a cancer of the white blood cells that though slow growing could be fatal. i will be happy if you're 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 diagnoseness the summer of 2011. as with so many cancer diagnoses, the education began suddenly and unexpectedly. after a day or so of sharp, excruciating kidney pain, eichner, a single parent after teenage boy, drove himself to the emergency room at his local hospital in olympia, washington, where he had been living at the time. his sister-in-law, a trauma flight nurse, had told him she thought he had kidney stones, so eichner was expecting to be admitted for a standard, albeit painful

procedures procedure, but 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've got what we believe is leukemia. a blood test soon revealed that eichner, in otherwise perfect health, had cml. the excess number of white blood cells contained in the sample confirmed that much. the doctors explained that the stabbing pain he thought came from his kidneys probably was from his spleen, enlarged by the high concentration of leukemia cells within. although the slow moving of the disease meant he wasn't in danger, he needed to start treatment right away. as eichner was rapidly informed, danger could eventually come. if the treatments didn't work, within five years, his

bone marrow with full with black cells, white blood fails that fail to mature, and those are both overly abundant and useless. his blood, once free flowing would turn into sludge. the supply of iron-rich red blood cells would steadily plummet, leaving him fatigued and neming, while a decrease in the number of platelets would render his blood unable to clot. as the disease progressed the capillaries leading to ice eyes and brain would enclosing. his spleen would likely become profoundly enlarged. as his body began shutting down he would bleed in his brain, in his intestines and out of every or fist. 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 long needle to break through his bones, which had become hardened and en flamed from the perfusion of white blood cells within. finally, she managed to extract an ounce of marrow, the spongey matter in the center of our bones where new blood cells are made n. the genetics laboratory, a flourescent dye applied to the dna in his blood cells revealed the tell tale sign of cml, a genetic mutation known as the philadelphia chromosome. an abnormal osterman regarded as the final feature of this fatal, spontaneously arising cancer, and discovered more than 50 years ago. 20 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 a doctor named brian druker right away. don't do anything before you

see him, the friend told eichner a couple of days after his diagnosis. three days later, eichner got a call from druker, who mysteriously, eichner didn't know how, gotten his phone number. during the next 20 minutes druker talked eichner down from panic, assuring him that being in the early stages of the disease, eichner could wait a week or two before making the trip south to oregon health and science university, where druker had been treating and researching leukemia since 1993. he gave eichner his professional blessings to go drink beer. it was august, and eichner had been getting ready to leave for a day at olympia's annual summer brew fest, his brother's idea of getting his mind off leukemia for a while, 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 has been instrumental in developing, a drug aimed at tackling the cancer at its root. so, i won't leave you in suspense. this is just the beginning of the book. gary eichner is still alive. in fact, he was supposed to be here. i was hoping he would walk in right after the excerpt. yes, so six months after he began taking the drug that i write about in this book, his tests came back 0 out of 20. so you remember i said when he was diagnosed he was 20 out of 20, meaning, in the sample of cells taken from his bone marrow, 20 out of 20 contained this genetic mutation called the philadelphia chromosome, so six months after taking this drug it was 0 out of 20. so, i would like to start with that excerpt, because i think it shows so much about

why this story is important, and why i love it so much. because of the impact that scientific progress has on our lives and this unstoppable drive that we have to make tomorrow better than yesterday, and the lengths that people will go to, to ensure that that progress happens. when i first began researching this story, i didn't know that it would be like this. i was working at a medical journal in the year 2000, and i would hear this word, the philadelphia chromosome. it was when data was starting to emerge from some studies, and i didn't know what it was, but the name is very captivating. it's a great name for a genetic mutation, the philadelphia chromosome. years later, i became a freelance writer, and wanted to dig in a little bit more about this story to understand what was it, you know, maybe there was a

magazine article i could write about it, and i started talking to some people, including brian druker and some other people that i knew by that point. and my research began with a question of why is it called the philadelphia chromosome, and as you might have guessed, it's called that named after the city where it was discovered in 1959. two scientists, peter knowle and david hungerford were researching knows. peter had stumbled upon this method for expanding cells more than they had been expanded before. because he was in a hurry, he was very anxious to cure cancer, actually. he was young and ambitious and thought he could do it in a summer, so he rinsed the cells under tap water instead of the special laboratory water. the cells ballooned out and suddenly he could see

chromosomes just a little bit more than people had been able to see them up until that point. this is in 1959. compared to what we have today, it was still coat coarse, but it was something different. peter knowle was not interested in chromosomes. at that point there was no knowledge about the connection between genetics and cancer. no one was looking for the cause of cancer in our genes, but he figured, well, someone is going to be interested in this, and as i turned out, that someone was david hungerford. it was fortunate because david hungerford was also in philadelphia. he was should very old school sign tissues just loved to observe, loved to look through the microscope day after 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 knowle and looking at chromosomes through the microscope and one day was looking at some cells from a patient with cml and noticed that 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 actually on the cover of the book. obviously it was much typeier what he saw, but it with a this. chromosome 22. in 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 with a was going on was the cancer causing the mutation, was the mutation causing the

cancer, was it kind of 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 just thought it needs to be written down, and i'll give you an example. ok. so, we have in our cells a protein called kinase. that's a type of enzyme, and it sets things in motion. it's kinetic, and one time of kinase triggers the production of white blood cells, and it happens in a kind of stop and start way. our bodies don't always need to be making white blood cells, so the kinase is sometimes giving the signal

and sometimes not, so red light, green light. ok? now, that's the normal kinase, but with the philadelphia chromosome mutation, the kinase that triggers the production of white blood cells is mutated and in that mutated state it goes haywire, and it's always triggering the production of wide blood cells will it's a green light constant, so i wanted to understand, well how is it known that kinases were even involved with cancer, and i spoke with a man named ray ericson, who was the first scientist to uncover the connection, to find the involvement of kinase in cancer, and i said, how did you get there? why were you researching kinases? he said oh, ways researching a gene called sarc, and i with a looking for the protein products of a gene called sa --

src. i said why are you researching src? he said that was a gene involved in chicken cancer. why were you researching chicken cancer? he used to get made fun of researching chick than cancer in the 1970s and the story went like this. src was a gene involved in a virus that caused cancer in chickens, and when he went to find out, well, how did it cause cancer in chickens was when he uncovered the role of kinases. and where that gene had first been found went all the way back to 19 10, 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, so this is a true story. in 1910 there was a scientist named peyton who was researching at

rockefeller institute, now called rockefeller university in manhattan, and he got there in 1909. he had been researching for a year, and one day this woman shows up at his lab carrying a chicken with a tumor sticking out of its belly, and the true story, she says she was a farmer, she walks up to his lab, she looks at him and says, can you operate? can you operate? he says sure, ok. why not? so rockefeller institute had its first ever chicken surgery, and he removed the tumor from the hen. unfortunately, the hen did not survive. there were remnants of the cancer in its body, and it died. but, now peyton raus had this tumor and figured, you know, i've got to reseventh. i'm not going to waste this,

so he creates an extract from the tumor and takes that extract and injects it into another chicken, and the chicken got the same cancer as the first one. he thought ah, cancer is contagious, contagious chicken cancer. and what was important about this story is not so much that peyton raus had 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 genetic underpinning of cancer, a cancer can begin in our own genes, because it turns out the culprit gene in the chicken virus had come from the chick than itself. and that was led people to understand that our -- it can happen in us, right? which is if you think about it, just a preposterous notion, because how and why

would our healthy dna undergo a mutation and in that mutated state trigger something that kills us? and i just, i loved that story, to think that our current understanding of cancer goes all the way back to this farmer, who brought her chicken to a laboratory to undergo surgery, because first of all, it would never happen today, right? the paperwork alone, she would just say, i don't need the chicken. 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 were some people who started to think, well, could we make a drug that targets that, right? could we make a drug that blocks that haywire kinase that stops the cancer at its root cause? this type of drug had never been attempted before. it had never even really been thought about before. and of course, one of the people asking that question was brian druker, and he worked with people at the time in the pharmaceutical company at the time it was ciba-giegy in switzerland, who was asking, could we make a drug stopping cancer at its root cautious and after working in chemistry a couple of years, which is a

fascinating story in its own right, they had a few compounds, and they sent them to brian druker, who by then was here in portland, to test in his laboratory, and they didn't tell him. they sent him five. they didn't tell him which one they thought was going to work against cml cells, so he tested them in the lab and right away could see one of them was killing the cml cells. so then he can the -- did the same thing, he gave them to his students, didn't tell them which ones were working, which one was the one, and the same thing happened. so, you would think having seen that result in a laboratory that the pharmaceutical company would move rapidly to the next step that would be the normal thing. having seen such properlyness the lab, the next step would be animal studies, and if it was proven safe in animal studies, human trials. but what happened after

those initial tests were done, everything ground 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 shefed? -- shelved? there were a few things i found out first of all, there was the risk, ok? i told you this drug had never been made before, had 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 is with aing going to be one sick patient. it was a risk. you don't know what's going to happen when you give it to people. tragedy and disasters like what happened with thalidimide, this was a drug that was supposed to help women cope with pregnancy, and it deformed their babies, and nobody wanted an event like that to occur, and york zimmerman, the chemist that made the compound said to me, you know, you can look at this drug and say, why did it take you so long, why couldn't you get us patients faster, but if we had gone faster to clinical trials an something happened, you would say, why did you 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 was tested on animals. they moved into animal studies after some delays, and it was tested on mice and rats and dogs and rabbits and monkeys, and hamsters i think and some other cell lines. and there were problems at one point in dogs. some dogs were experiencing liver toxicity, and brian druker got the message that there were these toxicity problems. they were not sure about whether the drug would be moving forward. a man named alex matter who was at the drug company leading the drug development program at the company was hearing from a toxicologist conducting the animal studies, over my body will this compound go into man.

but brian druker is saying, well, ok. there's liver toxicity in cost. -- dogs. fine. you have to give this drug a chance. you're giving dogs 600 milligram doses of the drug. a clinical trial starts at 25 milligrams, and we know the signs of liver toxicity. we are doctors. that's what we do, and a clinical trial, that's the best health care a person can get is in a clinical trial. if there's a problem happening, we will see it, and we will stop the drug. we are not going to keep giving it until they have extreme liver toxicity, right? give the drug a chance. but that wasn't the only problem. the other issue was the money. cml is a rare disease. it's 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 about 230,000 people per year in the united states. all types of cancer 1.6 million people per year in the united states. ok, so 1.6 million, 5,000. the drug company could not see how they were going to recoup on the ininvestment. the patient population or the market as it's called was too small, and they were looking at that through the eyes, through the business model of chemotherapy, which is given for short amounts of time, usually. so they couldn't see, how are they going to recoup on its investment. so much eventually the drug did go into a phase one

clinical trial that started 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 a hematoligic response. their blood was returning to normal. normal white blood cell count was 10,000. people could come into doctors with counts up to a hundred thousand and after a few months were back in the normal range. it was unprecedented, but even at the phase one study, even when those results were coming in, there were still delays, when it was going to move from phase one to phase two, because all 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, and actually this is one of my favorite moments in the book. of the story. so there was a patient named ceus mcnamara from toronto and with a was happening when the phase one trial was going on, it was perfectly timed with the rise of chat rooms. couldn't have been better timing, so cml patients, to find support, right, to find others going through the same thing you're going through, it's a rare disease, so you're not going to find many people in 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, which was the primary drug given to patients with cml, which is a very harsh drug, or having been through a bone marrow trance plan taste, which is another extremely harsh procedure, still the only technical cure for cml, but that's if you survive it, which is about a 50% chance, and if you're eligible for it, and if you can live with the side effects, which can last a lifetime, so susan mcnamara was very sick, and she was base lick living between her bed and her computer two feet away, and she would go on the cml chat rooms and be reading reports from people in the clinical trials post bg how great they felt, that their blood counts were back to normal,

that they were having this incredible response to the drug. so she emails brian druker and asks if she can get on the study, and he says, i'll put you on the waiting list, but his waiting list was 100 patients long, and every time he got a new dose of the drug, he got permission to add another patient on the study, he had to choose which was the sickest. so he says, i'll put you on the waiting list, but i don't even know whether this drug is going to be made. i don't know when it's happening. i don't know when the trial will open in an expanded way, i just don't know, and maybe can you do something, and she said to me, 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 i was not going to get, and she wrote a petition.

it was signed by hundreds of patients within weeks, sent it 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 this story that i just get this needs to be told. because 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 pulls back the curtain on how medicine gets made, on the science that goes on, on the politics that go on, to equip our self with did

knowledge so that when we as health care consumers think about the world we live in, we know if facts of what goes on. but also, not only to tell the story of this miracle drug, but also to tell the stories of the miraculous lengths that people will go to, to ensure that their vision that, their belief gets a chance in this world. so, i wrote the book, and that includes the talk portion for now. thank you so much. and i will invite brian druker up for any questions that you might have. we'll sit over here and be happy to answer your questions. [applause] >> thank you.

ok. >> thank you for coming, yes california. i have a question. did the disease cause 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 are they completely different kinds of diseases? >> would you like to start with that? so, i mean, that was a question when nothing was known, right? i mean, 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 gentleman to my right, that that is one of the major questions now is

when these mutations are found 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, but i would ask the current. >> the current view of cancer is that every cancer will have a driving abnormality, something that's broken that's driving the growth of the cancer. as you just pointed out, a lot of the cancers carry a lot of additional abnormalities that have nothing to do with it. they're just what we call passengers. so the terminology is they're drivers mean they're actually driving the growth of the cancer and passengers who go along for the ride. we have to understand the differences which the drivers are, because those are the ones that get targeted with the drug like glevac that see remarkable responses and change the way

we think about cancer and its treatment. >> it's a layperson question, but you said that, i thought you said that the chicken story, it was a virus that caused the mutation, so that's one question, and the other thing you said is that when the chicken died, he took the tumor and injected it into another chicken, so you said actually cancer is contagious. >> mm-hmm. >> but how else is it contagious? how does the tumor get from one place to the other? because here it was injected. mm-hmm. >> two questions there. >> clarifying what you said. >> so, that was in animals, right, and was a virus, ok, so it's a virus that's contagious. viruses are contagious. the physical matter of a tumor is not.

it's just matter. so, in people, cancer is for the most part not contagious. there's not contagious cancer. there's human papilloma virus can lead to certify have i cal cancer. about 20% of cancers have a viral connection. i think that's the right 20%. >> 20-30 worldwide hepatitis with liver cancer. 20% of the u.s. probably. >> ok. so, for the most part, it's a phenomenon of the animal world, and so what he had, what peyton raus had proven when he ground up that tumor and injected the purified extract into another chicken was that there was a virus in there. that's what he was showing, and he was studying the vy rurx and it turned out the

viruses are wonderful to work with in a lab because they contain usually just four or five genes, and they could over the years later take one out, was it still causing cancer, right? and if they took one gene out, and the virus did not trigger cancer, then 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 was amazing about the experiment that paint raus did, he actually took the tumor grounded up and put it through a filter so no cells could get through. so it was no tumor cells, just this extract with no cancer cells in it, and he injected it in a chicken and that got cancer because it was a virus. what that virus did was it picked up a gene inside the cell, a normal cell of the chicken and changed it around so that it gave those cells a growth advantage,

and that became the template for understanding that genes, if changed around, can become stuck on the green light to cause cell growth. now, what's so amazing is that for 50 years nobody believed peyton ra -- raus. he said you probably got some tumor cells an that's what happened, but in the 1950s when they could culture these viruses in a petrie dish, people realized he was right, and in 1966, 55 years after this discovery, he won the nobel prize for that work. >> yeah. >> and he was the oldest living nobel prize winner, and it has a lot to do with the fact you have to be alive to win a nobel prize, so he lived a long, productive life that set the groundwork for the modern eastern era of cancer

genetics. >> and i think it was just a few years later that the nobel prize was given for discovering -- was awarded very soon after. the time also are kind of amazing. questions, yes. >> can't wait to see the book. it sort of reminds me of the book by rebecca [name] about cancer, not only the science and the personal patient history, but the sociology of the story of cancer and medicine, and so, i'm really interested in learning more about that, and i have a very good friend who is a

cancer survivor and has taken glevac for the cancer that she had originally had, and so she's been surviving very well with glevac. and so, i just wanted to say that i think that this is a great story for the repercussions on family, because i'm a person that has lost someone to cancer, and my friend, who is a cancer survivor with glevac, she lost her husband to brain cancer, and sometimes i think of cancer of sort of like divorce, the effect it has on families, cancer can cause families to implode, and the beautiful thing is that my friend, who was a widow raising these children said look, you have to live, so she got her doctor to give her glevac for her gist cancer even though she didn't have leukemia. so that was a great story

from just personal experience in san francisco at ucsf, and i think it's wonderful these breakthroughs that come that are not led by institutions but by individuals trying to just, as you say, these miraculous leaps by individual efforts. >> yes. >> so my question was, sorry, i do have a question, is that are there many patients taking glevac for other cancers besides leukemia, and especially how many gist cancers have been treated with glevac? >> do you know the exact numbers? >> the numbers for her gist, which is a groenl -- gastrointestinal tumor is about 3,000 a year, and a quarter will be treated with glevac so quite a few are on treatment. glevac has been approved for ten different cancers, an it

gets into one of the critical issues that jessica was alluding to, and that's that we define these broken parts that keeps that green light stuck on, and we are finding that sometimes what's causing the green light to get stuck on the leukemia tuesday on an intestinal tumor or skin tumor or other cancer and we can use the same drug in other cancers and that's why they are seeing a return on their investment because they can see -- use this drug on different cancers. >> on a mole dollar -- molecular level, how does glevac operate? >> as jessica noted, there are these enzymes, and there's off and on switches. they turn things on, and

they turn things off. and these enzymes bind what's called atp, and for biochemistry, you remember your high school biochemistry, that's the energy exchange system in our body. if you want to pay some money and the body uses atp, and what these kinases do is bind atp and transfer it to another protein, and that actually triggers cell growth. >> [inaudible]. >> we will get to that in a secretary. the way glevac works, one particular kinase it blocks the body atp so it captain trig ter signaling so it can't turn anything on. you might say atp you might say a dollar is a dollar and how are you going to have specificity? the reality is there are 500

different kinases in our body, and they all have slightly different structures, and we now have the crystal, three dimensional structure of hundreds of these different kinases, and they all are a little bit different, but the reality is there's no one of these drugs that shut down one. they off times 2-50 depending on what they look like. >> is it 300 abnormal kinases? >> there are 500 kinases in the body, and probably 300 of them have been shown to be active in cancer in one way or another, and they're one of the most commonly what i call drug targets in the drug industry right now, because they're so commonly mutated in cancer, the drug companies know that they can actually make these drugs, and there's been a successful paradigm with glevac and cml.

>> of the all the sarcomas whatever, how many of them have viral triggers? do they know, all of them? >> it's actually very few, somewhere in the range of 10-20%. >> i see. >> will have some viral triggers. >> i think you probably answered part of my question, and my original question was, how could you tell early on or how did people teller i on that that kinase would be the big target and then how could you tell that inhibiting the kinase would be specific, and to pull out to what you said, is the different kinase is a common pathway for cancer in general? koup comment on those things? >> well, first of all, kinase is a pathway for cancel. they regulate cell growth,

and that can be a target to get stuck on in jessica's green light analogy. the way we knew that this particular enzyme was the right target goes back to the philadelphia chromosome. it's present in every patient with cml and basically defines the disease, and when it was discovered, and again jessica does a fabulous story going back to the '70s and '80s of the researchers who contributed to the identification of this kinase that comes out of the philadelphia chromosome, and when i came into the story, i went into the laboratory, and i said, well, if you make some ks changes to the kinase to make it completely inactive so it can't function as an enzyme, what does that do when you put it into a cell? and it does nothing. the active kinase, you put that into a cell and the cells grow like wildfire. you put them in tumors, you make a mutation that makes it an inactive protein, it

does nothing, so clearly to me that was the right target. >> i'll add one thing with just from the history that was so interesting to me was that when people were first researching kinases before there was an interesting of their role in cancer, there was like 5-10 kinases known. there's a man named sir phillip cohen from england who told me all about the research, and he said, we knew nothing. these were interesting proteins that had roles in other ailments. but when the role that they play in cancer was uncovered, you know, it's kind of like this lighted bulb moment of, of course, it turns out it's the perfect way for cancer to happen, and with the atp process that doctor druker describes, you can think of cancer as being incredibly

efficient, you know, as he put it to me, it's this 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% of viral generated. what about environmental factors generated, and are there just cancers that start just purely spontaneously without any outside actors on them? >> i guess it depends on what you consider environmental. but if we start and sort of track the most common, smoking, 30% of all cancers, and how does it do that? the way it does it is it just cells in the lung lining, causing them to grow, and any time you grow, you'll pick up some mistakes. but in addition, there are

chemicals in cigarette smoke that damage dna, and damaged dna, as we've been discussing, if the right place at the wrong time, you've got cancer. so, anything you think about any environmental cause, it's going to be things that damage cells, cause them to grow or things that damage dna directly. and the estimates range anywhere around 5% will be environmently caused. it may be more than that. it may be less than that. but that's kind of the average i've seen from a number of studies that have been done. i think if we are going to approach, the other reality unfortunately, i see cancer as a genetic disease, meaning it's caused by changes in genes, and any time our cells divide, they make mistakes. it just happens, and we have almost one trillion bits of information that have to be replicated faithfully, and there are going to be mistakes. and as we get older, these

mistakes accumulate in the body, and if you look at the numbers who get cancer, it rises very steeply after age 50, and to me that's just an accumulation of mistakes over time.

the. >> when does a drug finally did go to the fda it was the fastest approval ever. it was at trial to a half years but the entire development was 18 years. normally it is between eight and 10 so what took a long time was not the fda. a key and me but not in this case. when it is known to be when there are no satisfactory treatments available where it looks promising, there is

mechanisms in place where all of these designations about to is more face time with the fda. if somebody wants to work later hours they will that is what really boils down to. of the fda will meet with the drug company in a dance to say this is what we need a and everything is laid out as soon as possible now trying to put in place of bureaucracy is just a killer. for example,, it is problematic to use to experimental drugs as a clinical trial. you would think there is tories -- always experimental drugs if there is going to be cocktail's then move along but you cannot use to experimental drugs in a trial