>> thank you very much. here about 10 yearsago, i think sauder [assumed spelling] and i gave a talk together and i told the audiencethat a lot of times people confuse the two of us because we both have these long noses[laughter], and the thing is, that was good for me then because he is the more famousmyeloma doctor, but now it is like he has--we both grown up, we both have glasses, his glassesare right at the tip of his nose, and mine
multiple myeloma cancer ribbon color, are-i guess he got some extenders, becausemine don't reach [laughter], okay [laughs]. and so i share a long nose with him, but ialso share something i realized with dr. nuca [assumed spelling] here, and that is my pantssize. so about a month ago we were at this international conference in scotland, andi realized after i got there that i had flown,
i like to fly easy in a track suit, that idid not take any trousers [laughter], and so the first day, i kind of, you know, hada suit coat on top, and kept my track suit at the bottom, and then i said the next dayi'm going to go and buy some trousers for the remainder of the meeting, which was justone day, and then at 7:00, i wasn't even awake, dr. nuca calls, and he says "my wife has packedfour dry-cleaned pieces of trousers for me today," you know, "would you like to try one?"and it fit. okay. so having said that we will go ahead and get started. so we are goingto talk about relapsing and refractory disease. i'm not going to have too many slides withwhat do you call graphs and figures. i'm just going to give a broad brush, you know, overviewof where we are, and a little bit about where
we are going, obviously doctor, i think, loneal[assumed spelling], is going to talk more about some of the new and upcoming stuff andclinical trials. so just to say relapsed and refractory disease, they do have some, youknow, slightly different definitions. relapse is recurrence after response to a prior therapy,whereas refractory is you're progressing on the ongoing therapy, and relapse refractoryis you're progressing on it or within 60 days. so there are all these fine points just to,you know, explain the title of the talk. so the question is, when you have a disease relapse,the first question is, when do you reconsider treatment? does everybody whose disease iscoming back need to switch treatment if they are on treatment? like maintenance? or dothey need to, you know, just be observed.
so clinical relapse, which is defined as,you know, you're getting new bone mutations, you're getting more renal insufficiency, you'regetting new anemia, you're developing new bone lesions, i think nobody discounts thatyou need some kind of change to your therapy. the question that arises which is very commonin your first relapse, which we often call a biochemical relapse, where there is, notyet, nothing going wrong physically and the labs are looking good overall, but it is them-spike that is starting to rise. does this patient require a change in therapy? and often,that has major implications because often patients, these days, are doing very well,especially the first time, of first relapse, and if it were not for the m-protein tellingthem that their disease is starting to come
back, they're working full-time, and sometimesswitching therapy means starting to have to come to the doctor's office multiple timesa week to get intravenous drugs. so it is not a minor inconvenience, sometimes. so biochemicalrelapse, patients with asymptomatic rise of their m-protein can be observed to determinethe rate of rise and nature of relapse, especially with the first relapse. as you get into moreand more lines of relapse, third, fourth relapse, i think more people would be tending to treata biochemical relapse, because we know at that point sometimes waiting could put onein trouble because suddenly patients can get sick. however, patients with non-aggressivedisease or high-risk disease, those that perhaps had a kidney problem, renal failure, at timeof original diagnosis, if they're starting
to have a biochemical relapse we have probablya little more vigilance, and perhaps a lower threshold to restart treatment. but this isas much art as it is science. and there are some guidelines in the literature for doctorsthat have been introduced a few years ago, that said that if you have say a doublingof your m-protein on two consecutive measurements, separated by less than two months, or youhave an absolute increase or a gram, then perhaps you should consider treatment. butthis is, again, not based on too much scientific evidence, but just serves as guideline, becausethis is a common question that not only patients, but even physicians in the community ask experts.so what if you do decide that you need treatment, there are several factors that one has toconsider in treatment selection. and these
are disease related, related to the priortreatment, and also patient related. so the disease related are, what is the durationof response to your prior therapy? if a patient had a good response and then were off treatmentfor a long period of time, going back to the same treatment makes sense, in contrast toif you are off treatment for say a month, and your disease starts coming back, perhapsgoing to something different makes more sense. the cytogenetics, the chromosomal profile,which you heard, can also give us some clues as to which drugs may be the better ones touse. as regards prior treatment related effects, how did you tolerate the prior treatment?if there were side effects, neuropathy being one of them, sometimes for suppressed counts,are you going to be able to use the same drug?
or do you want a drug with a different toxicityprofile? did you progress after a prior transplant? then patient related, again, toxicity, age,general health, so there are a lot of factors and it is no one, you know, answer that fitsall. in fact, myeloma is probably among all cancers very heterogeneous in the approachto treatment, not only differences between physicians, as you heard, but also differencesfor what a patient does for each individual patient in his practice. so the options forrelapse and refractory disease, if you decide that you want to treat, again, when did yourelapse from your prior therapy? if it is less than six months, a lot of patients wouldsay try a different therapy. a stem cell transplant, if you've not had one, or as dr. wiesel [assumedspelling] was saying, if you've had a transplant
and gone fairly long without need for anytherapy, then another transplant. if you've had more than six months off treatment thenyou could repeat the initial therapy, provided you tolerated it, and it did well for youin the past. or consider a different therapy. again, stem cell transplant, if it has notbeen done, or you know, there has been a sufficiently long time. and then clinical trials, onceagain, a pitch that dr. wiesel made, the clinical trials, perhaps should be, you know, at thetop there. because that is how we come to all these options that we have today. so thisslide has already been shown. it is a timeline to show that we have certainly come a longway. from the era of somewhat modestly effective therapy, to therapies you are seeing, areproducing much better responses. i just have
four or five slides on the licensed agents.you heard about all these this morning, so i am not going to go into great detail. butlenalidomide, approved for relapsed refractory disease, and also more recently for patientswho have untreated myeloma, if they are not transplant eligible, but these are the fdalabeled indications and at least, in the united states, we have been allowed so far to usethis drug somewhat liberally in contrast to europe, where despite the approval recentlyin europe, there i still debate on whether they can afford the drug to be given in asocialized health care system, bosutinib, likewise, the backbone of a lot of agent regimensthat you've heard about this morning. it has, again, overall single-agent response rateof 43%, but you can combine it with other
drugs, and get much higher response rates.the issue of it being a better drug for perhaps high-risk myeloma is something that is especiallyfor 414, i think, increasingly looking through, and in certain situations, these 17p delineationsseem to respond perhaps better to this agent. and once again, you know, this drug has neuropathy,as you know, as the major side effect. kyprolis or carfilzomib was approved now about i guesstwo and a half to three years ago, and this was approved for patients who had failed priortreatment with bortezomib and immune-modulatory drugs, and had, as a single agent, a 23% responserate, but when combined with other agents, it has achieved response rates in excess of70 to 80% with some complete responses as well, and there have been trials done evenin frontline therapy with this agent now,
and it is looking very promising, though itsuse in frontline is still not widespread, but could change in the future. and then pomalidomideor pomalyst was approved a few months after kyprolis, so it's been a couple of years roughlyas well, and this, too, has a similar single-agent response rate, as does kyprolis. it is a pill,so that is one advantage of it. and these are drugs that are in the same class as pomalidomide,as lenalidomide, and thalidomide. the immune-modulatory drugs. and most recently, as you heard panobinostatwas approved just literally a few weeks ago, just hit the market, i think end of march,and this is approved for combination with dexamethasone, as about a 60% response rate,in a separate trial patients who were progressing on bortezomib and dexamethasone seemed torespond when this drug was added to the mix.
and so this certainly offers a new option.however, the fact is, there are some genuine toxicity concerns, especially diarrhea, countsuppression, that have made, you know, some physicians somewhat leery about, you know,using this in untreated and less-heavily treated patients. how this drug pans out, i think,we will know over the next year or two, as other trials are done. and it could probablybe used in combination with other drugs, other than velcade, where it probably has more potential,carfilzomib, which was a trial that was done here at emory, and then other drugs like revlimidand pomalidomide, so we will see how this drug pans out. but just after having, youknow, said, you know, just reiterating the names of the drugs, we are just going to givea brief overview of some of the, you know,
controversies in the field, and some of thepotential in the field, with agents. so what we have learned is the immune system is veryactive in myeloma. this was something alluded to by dr. wiesel, when he talked about thepotential for iatrogenic transplant to potentially cure up to perhaps 15-20% of patients withmyeloma, and that is the first proof that we had that the immune system may work inthis disease. the immune system, we are realizing now, is very powerful. you're probably readingin the lay press about these new miracle drugs, these checkpoint inhibitors, that are showingactivity in a wide variety of cancers, including things that were heavily pre-treated, resistantcancers like melanoma, and lung cancer. in myeloma, we also know that the immune systemis powerful, because our drugs, thalidomide,
lenalidomide, and pomalidomide at least inpart worked by boosting the immune system, and they do have direct effects on the cancercell, but it is felt that a lot of their effectiveness is by boosting the immune system to eradicatethe cancer. so i think that this is an area where there is a lot going on in multiplemyeloma, and we are starting to see some of the things now perhaps in the work of approval.and the antibodies have been alluded to. i think dr. loneal will probably talk aboutthem. so these two are the two prime molecules, elotuzumab and daratumumab, and this is, theseare drugs that are actually going to be presented at one of the largest international meetingstwo weeks from now. so does anybody know who is going to give the elotuzumab presentationfor the world-wide trial? dr. loneal. and
derotimomab is going to be presented, anddo you know who is going to give that presentation? dr. loneal. so all these drugs are thoughto perhaps present the potential for the next big leap in survival of myeloma, and thisis going to be, i think, two drugs that will hopefully be fda approved within the nextyear. so but the controversies in myeloma are, you know, several. and one of them isdo we go hard like an ironsmith, bang away with one big, you know, hammer? and kill offeverything hopefully right away? or do you go like a goldsmith, and with a smaller hammer,and keep banging away repeatedly? and this is a controversy that i think still refusesto die down. the data seems to be starting to gather pace for the ironsmith approach,but i think that it is not crystal clear.
okay. this is, again, i did steal from dr.loneal, as well, so as regards the depth of response, you've seen this slide. this hasbeen explained to you by two previous speakers. that what we know is that we are now achievingdeeper and deeper responses. and it appears that this category of, you know, molecularremission, may in the future be something to strive for. there are data starting toemerge that it may be a surrogate for better long-term outcomes, like survival. what wedon't know is whether it is a reflection of the biology of the disease, or if it is trulyan end point to strive for. there are data starting to emerge that it may be a surrogatefor better long-term outcomes like survival, but we don't know is whether it is a reflectionof the biology of the disease, or whether
it is truly an end-point to strive for. whati mean by that is that we know that if a person gets four months of treatment and achieves,say, a conventional cr, and another person gets four months of treatment and achievesa molecular cr, the person who achieves the molecular cr is likely to do better than theone who gets just conventional cr. what we don't know is whether that patient who isin a conventional cr, whether we should give him more treatment to get him to that lowerlevel of response, and whether those people would then do equally well. or is it justbiology? those who get there quickly are destined to do better no matter what. so this is adilemma that i think will hopefully sort out in the future. so how deep to go, how whetherto go with all our drugs at relapse, whether
to give it in serial manner, whether to godeep and in deep, and the other thing is, do we treat it like a chronic disease? andthis, again, was a controversy that was highlighted by dr. wiesel earlier, that you know, a lotof drugs do look better in terms of improving what we call the progression free survival.that you start a drug, and you take longer to progress. that is what is called pfs-1.obviously the gold standard is that you want to improve the survival. and a lot of timeswhat happens is it is felt, or historically has been especially felt that if you use allyour ammunition in pfs-1, that it is going to be very little left to give afterwards.so recently people have started talking about pfs-2. that is you look at not only how wellyou do with your first line of therapy, but
also with your next line of therapy, add themup, and see if that is better than pfs-1 plus therapy afterwards. and this has now beenaccepted in europe as a surrogate for survival. it is something that is getting increasingtraction here as well, and some data, you know, does suggest that if you use all yourdrugs together, you are not only impacting pfs-1, but also pfs-2, and overall survival,but then there are some other data sets that refute that. so we still don't know whetherwe should treat it forever, or give a break, as dr. wiesel said, get patients off treatmentfor three years, come back on. so there is still some controversy in the field. and then,as far as drug development goes, what we call empiricism to rules. which means that historicallydrug development has been that you have a
drug like velcade, for that matter, revlimid.you know, the drug was discovered, the company said "let's start treating some cancer patients,let's see how it works." so you enroll in a trial, 10 patients with lung cancer, 10patients with breast cancer, colon cancer, myeloma, and then you get a hint of a theorythat patients with myeloma are starting to do better, so let's do a larger trial in myeloma,and then it seems like it works reasonably well and that you get a large trial to getit approved. so that is the path that all the drugs literally that we have today havetaken. that you have a drug that works in myeloma, and then you spend the next 20 yearsafter it has been approved, to figure out why it worked in the first place. and thatis where we are with revlimid and velcade,
we still don't know why they work. so butthey work. so that is a paradigm of drug development that we are trying to move away from, andthat is where this really hot topic, these days, it is all over the press, there is newstrategies to win the war, personalized medicine comes in. and that is trying to get treatmentsthat are specific to each individual patient. we do somehow practice personalized medicinein a way already in that we decide for a patient whether their age, their other health problems,their side effects, allow them to get a certain therapy. so that is one kind of personalizedmedicine. but we are talking about personalized medicine based on the genetics of the tumor.and so you heard again this morning that we have kind of gone and found out certain chromosomalabnormalities that seem to do better than
others. but you know, when you look at chromosomes,it is like taking a telescope and looking at mars. you just get some basic idea. thenyou do the fish testing, which is a little more powerful, instead of looking at 20 cells,you're looking at 200. that is like launching a satellite to look at mars and seeing ita little more clear. then you come now to a new generation of tests, gene expressionprofiling. you heard it was something that tells you what kind of proteins perhaps thecells are going to make. but the real answer, a lot of people have felt, historically atleast, lies in the dna. which is really what makes the chromosomes. so getting there islike actually landing, you know, a pathfinder on mars, and actually seeing what is goingon. and that, i think, we are there now. and
what have we found? so the thing is that sequencingtechnology has become pretty ubiquitous. about 12 years ago, i think, the first human genomewas sequenced. it was a battle effort by solara genomics, and it was a federal effort, likeat three institutions. one was the sanger, in england, the broad at harvard, and thethird was at washington university, in st. louis, and it took 10 years. and it took overa billion dollars to sequence one human genome. and now technology has leapfrogged. the sequencerthat you see on the far left is representation of one of the most common sequencers usednow. it is literally a machine this big. it can sit here right on the table. and now sequencinghas obeyed, so far, what we call the moore's law of computing, in a way. moore's law saysevery 18 months your microprocessors get double
the speed, and your computers get doubly powerful.in sequencing, it has meant that with time, the cost of the sequencing has come down andthe speed has gone up. so instead of taking 10 years to sequence a human genome, you cansequence a human genome now in literally less than a week. instead of sequencing a genomein 10 years, i mean, instead of costing a billion dollars, the one thousand dollar genomeis here. the reagents and the pause to sequencing has evened out in the machine, doesn't costmore than one thousand dollars now. that is cheaper than getting a pet scan and ct scannow. the problem lies in what we call the bioinformatics end of the equation. so whenyou get the patient's blood sample into the sequencer, and it is turning that after aweek, you get data that looks like this, which
is essentially something that a computer guyhas to look at. and this data is one human genome produces one terabyte of data. whichis more than what a pc can hold. so you have to realize that to get information out ofthis, so there is data, then there is information, and then there is knowledge. wisdom, i think,can come, you know, even without data and information and knowledge, but the thing isthat you need to have several hundred people with a certain kind of cancer sequence toknow what is going on in the genome. so each human genome is about one billion base pairs,and if you need 100 people, you can imagine a spreadsheet with a billion columns and 100rows. so how can you even start thinking where in which cell in that spreadsheet to focusyour attention on? and that is where we need
mathematicians, and that is where we needbioinformatics people to really come in. and that is what adds another $9,000 to the costto sequencing a genome, and it becomes $10,000. and these people are in such short supplythat right now the problem is that we have reams of data. this is the, you know, genomeinstitute's computer center, at washington university. so as i said, the machines, theroom that sequences, so washington university will sequence 200,000 genomes this year. whichincludes everything from bacteria in your stool to a human genome, to animal genomes,to insect genomes, and what happens is that this all this data then goes and into thiswarehouse. and it sits there. because there is nobody there who can make sense of thedata. that is the bottleneck we are facing
right now. we have a lot of data, we can'tinterpret it. and so what have we learned though? so what we have learned is when westarted to sequence the human genome, it was thought that we would have 100,000 genes.because we are very complex organisms. look at it. we have 20,000 genes to 25,000 andmax. that is what we found out. which is less than is in a grain of rice. so that grainof rice has more genes than we do as humans. so that tells you that it is not all thatsimple as it was thought to be. it is going to be the mechanisms that have evolved tocoordinate these genes. the symphony of these genes, that is what we are probably havingto decipher. there is something wrong in the symphony sometimes, not just the individualplayers. so we are still, i think, but it
is an exciting time. and this is certainlysomething that is going to start to pay dividends. what have we learned in myeloma today? sothe thing is that there are a lot of genomes that have been sequenced, and now literallyevery cancer has had, the common ones at least, several hundred genomes sequenced. and asi said, we are relying on a lot of data. there are some genomes like leukemia, where theyare just 10 mutations out of the one billion that are thought to be perhaps important.the other genomes, like lung cancer, where there are hundreds of mutations. myeloma hasfallen somewhere in between. it is not as simple as leukemia. it is not as complex aslung cancer. but the problem is we found mutations, but none of them individually account formore than perhaps 5 to 10% of patients. and
so we have had our old approach of being like,you know, terrorists, going in and with an ak-47, trying to mow all the cancer cellsdown, and hoping that we will get a lot of it. we want to become snipers. we want topick out what is driving the cancer, and we want to shoot for each individual mutation.and that is where, you know, the difficulty has arisen. and we are going to hopefullyget there. but this is going to take very complex clinical trials. and what we havelearned, we have learned in myeloma that there are clinical tides, we call it the tide, coronaltide hypothesis of cancer. so what you see at the beginning, you see this is a patientwho was treated at the mayo clinic in arizona, and the patient, this is his cancer, and thecolor, i am color blind, so please excuse
me for that. so the thing is that there arethese different cells that are in the pie diagram, that are different kinds of mutationsin different cell types. some cells have mutations that put them in the red, and others haveother kinds of mutational profiles. so even within the cancer, either mutations are different.it is not only that your cancer is different than another individuals. even within yourcancer, there are cells that have one mutation, and some that have another. and so what happensis that the beginning, you start out with certain mutations, and you treat the patient.this patient gets, i think it is lenalidomide and dexamethasone. you can see over time thered goes down. and if you look to the end, the red is still down. so previously it wasthought that when people became resistant
to drugs, they got more and more mutationsin the same cell. but that is perhaps true, partly. in this patient, what happened isa very minor clone at the beginning, you can see the color, emerges toward the end as thedominant clone. and so what happens is that what was initially a response, has remaineda response. that cell is still gone, but a new kind of cell has taken over. and midwaythrough that chart, i don't want to go up there and point out, but at one point, theytried the same drug a second time because some cells with the original mutation werestarting to show up. and they had a response again. so, suggesting that you can maybe,if you have this kind of information possible in real-time, that you can predict what kindof mutation profile in a cell or tumor is
dominant at any given time, and choose yourdrugs based on that. this sounds like science fiction right now, but it is probably goingto be reality, perhaps, you know, within our lifetime and probably within the next decade.so these are technologies you have to sequence the cells one thousand times to be able toget this clarity. because once you sequence a cell once, you don't actually, you're notabsolutely sure you've done it right. and too, you don't get all the cells in the mix.so when you take a tumor and you sequence it one thousand times, is when you can tellreally with some big real certainty what kind of constitutional makeup that tumor has. soit is very complex. so it will be a while before we get there. this slide has shownthat we have relapses, and we've got, you
know, responses, the relapses get more frequentunfortunately at the moment, and you know, responses, the depth goes down. but thereis, as you saw, moves afoot, and the mmrf leads this effort. the compass study, it isone of the major examples of big data and patient centricity. again, big words thatare very popular. and to mine that data, and to try to make sense out of that data, i thinkwe are what you call getting there. but it will be a while before we can utilize thisinformation for any individual patient. and the next thing that comes up is what-how aredrugs going to be developed? so far, we have had a paradigm of blockbuster drug development.a billion dollars, and you've got a blockbuster drug. and that requires a certain number ofpatients to be able to take a drug, to sell
enough drug. but if, say, there are 25,000new myelomas each year, and only 2,000 of one mutation and 2,000 of another, and youneed to develop a drug for 2,000 patients a year, the economics are very different.and so how are we going to be able to support this drug development? these are dilemmas.there are orphan drugs that command very high prices. so it will be something that dr. lonealwill talk about as well i'm sure, how we get to drug development. but there is also increasing,what do you call? understanding. that perhaps we can even take information on what we callnf1 trials. so previously, what used to be is that if you had a drug and it producedresponses in only 5 out of 100 patients, the fda didn't approve the drug, because 95% ofpatients didn't respond. but what is forgotten
in that is that 5% of those patients responded.there was something for those patients that made them respond to the drug. so increasingly,now, those are becoming very important patients. where places are starting to sequence thegenome of those patients who respond to figure out what is their biology that made them respond?yes, the drug didn't get approved, but for them it could have been a possibility. sowe talked about personalized medicine. and then the next step is really precision medicine.some people equate the two. some see it a little distinction. so personalized medicineis, as we said, finding a treatment for your cancer. precision medicine is when you getto be agnostic to cancer type. you don't care whether you have lung cancer, breast canceror colon cancer, you just look at what is
the mutation. if that mutation is presentin colon cancer, breast cancer or lung cancer, it doesn't matter. you develop a drug to amutation. so, so far, historically the fda has approved drugs only based on certain diseasestates. in the future, it is felt that what is going to change is you are going to developa drug for a mutation, and as long as you have a mutation, if you have lung cancer,breast cancer, or myeloma, you can get that drug. so that is going to take a differentregulatory approach to drug approval. but this is in real time. this is happening. thesekinds of trials have been going on now for the last few years. and there are some, youknow, real success stories that are starting to emerge. i'll wind down, but this is a littledigression, but what is the story? so this
is lucas wortman [assumed spelling]. he isa mind at washington university. his story has been there in every major periodical.in fact yesterday it was in forbes. so he was a medical student, with me, at the v.a.,i was an attending at the v.a., when he developed a different kind of leukemia. acute lymphoblasticleukemia. he got chemotherapy, acute lymphoblastic leukemia in adults has about a 40% chanceof cure. unfortunately, his went into remission. when he was, then he chose, after medicalschool, to pursue hematology oncology training as a cancer doctor. in his first year of fellowship,his leukemia came back. and so he was actually attending on the bone marrow transplant unitwhen it was found that his leukemia was back. so he was admitted to that very unit, givenchemotherapy and a transplant. and he was
in remission. for the next three and a halfyears. then, the first year he became an attending physician, his leukemia came back again. sothen what happened is that he was given chemotherapy. this time, his chemotherapy just didn't work.so his colleagues, that is, us, you know, some of the people in the genome center, decidedto sequence his genome. it took a week to sequence the genome. and it was found thathe had over-expression of a molecule called flit 3, which is actually not thought to besomething you would imagine in acute lymphoblastic leukemia, which he had. it is something thathas studied with a different kind of leukemia called acute myeloblastic leukemia. and whatwe knew was that there was a drug that was approved for kidney cancer, called ceritinib,that would probably work for him. so it was
asked of the drug company that manufacturesthe drug, could you give him a free supply of ceritinib, we want to try to get his leukemiain remission, and the company refused. so his colleagues got together, it's an expensivemedicine, $10,000 for a month supply, and so got him the drug. and within 10 days, hisdisease had achieved a remission. he had a second transplant, and that was five yearsago. and now he still attends on the bone marrow transplant unit. so that tells youthe power of genomics. it is something that has great promise. it will hopefully be applicableto a lot more patients in the future. but also we are going to be facing another onslaught.we have going from guidelines that we are given are to developing pathways. that isthe next hard thing in cancer that we are
facing. that you are going to have to producevalue for treatment. so right now if you look at guideline authority, they tell you youcan treat a patient with this, this and this. in the future, insurance companies want youto put a price on the treatment, and justify why one treatment and not the other. and thatis called pathways. that, however, is going to be a fight that we are going to have tofight. so to summarize, relapsed refractory myeloma is treatable. patients typically receivemultiple lines of therapy. treatment sometimes can be continued for an extended period oftime. several standard options are available, and with the introduction of each new drugpotential for additional combinations arises. do consider clinical trials, once again. andwhat we are hoping for is that you are going
to come from an era of ineffective therapiesto therapies that produce these dips, these responses, before the disease re-grew. thisis something that we are going to learn from these genomics to finally cure the disease.and to put it in asterisk at the bottom, cure
in medicine is possible only in two conditions.one is infection, and one is in cancer. there is nothing else, be it hypertension, be itdiabetes, that we can cure. so we are curing cancer already. we need to cure myeloma. thankyou very much. [ applause ]
