♪ announcer: from our studios in new york city, this is "charlie rose." katie: good evening. i am katie couric filling in for charlie rose. in 2017, according to the american cancer society, nearly 1.7 million people will be diagnosed with cancer. over 600,000 of them will die. that is over 1600 deaths from cancer every single day. it is a matter that became deeply personal for me when my husband died of colon cancer in 1998 at the age of 42. that was 19 years ago. today, there have been a number of advances in medicine that have taken us a long way in the fight against cancer.

there are promising new breakthroughs giving patients and their families a reason to hope. in 2015, president jimmy carter suffered from late stage melanoma, a cancer once thought to be a death sentence. but after undergoing a new treatment, his tumors disappeared. and today, he is cancer free. how close are we really to finding a cure for cancer? to help answer that question, we are joined tonight by dr. bill nelson. he is the director of the comprehensive cancer center at johns hopkins. dr. louise perkins is chief science officer at the melanoma research alliance. dr. neil segal is the clinical director of the immuno therapeutics group. tom marsilje is an oncology drug discovery scientist and patient advocate who was diagnosed with colon cancer at the age of 40. you are an oncology researcher

working on lung cancer primarily. in 2012, you had the highest of highs and the lowest of lows. tell us what happened. >> i have always wanted to go into oncology drug discovery since high school. i had a lot of cancer in my family. i plan on that for many years. i started on industrial focus in 2003. i was passionate about it because i was an end of life caregiver for my mother and sister, who died of pancreatic cancer at a young age. i took it very personally and seriously, drug discovery for oncology. there is a lot of hard work and also luck in drug discovery. i was part of a discovery team -- part of a project team for lung cancer about 10 years ago now. i was coinventor of a drug that became fda approved.

it is a game -- a dream come true for an oncology scientist to have anything approved. there is a conference each year. it was presented by our clinical team, researchers at the clinical trial sites. it has shown an amazing response rate. i was walking on air. i felt i was helping my mom, so many patients. it was really kind of my one shot i thought at having success. by chance on the same day, i had a colonoscopy scheduled for about noon. i went for the colonoscopy. they knocked me out on it. they asked me on a scale of one to 10 about the anesthesia. i said 11. i had the spinal tap. i started waking up. i could hear the gastroenterologist who did the colonoscopy tell my wife, "your husband has colon cancer, we need to schedule emergency surgery." within a six-hour period, i went

from the highest of lies to the lowest of lows. earlier in the day, i was crying with my wife and said there are few things that scare me in life but cancer is one of them. it was june 4, 2012. i will never forget that date for the rest of my life. that is true of most cancer patients. they never forget the day they were diagnosed. based on my pathology i had , about a 30% cure rate, which is not great. but it is a lot better than zero. katie: i thought stage 3 had a higher than 30% cure rate. >> it was stage 3c. i had a lot of lymph nodes and invasion in my neurological system. stage three overall is much higher, but i was a worst-case stage 3 patient. as a scientist, i could look at the statistics myself. katie: they say you should not google anything when you are diagnosed. >> i did it immediately.

obviously, i was very upset and scared. really clinging to the 30% hope. it is not great but that is real hope. i went through chemotherapy for six months. i had a clean c.t. scan, did chemotherapy. my life turned around. i re-prioritized my life in a lot of ways. i felt like i had dodged a bullet. i was always relatively active. i became a long-distance runner. eight months later, i had my next c.t. scan and there were enlarged lymph nodes. they were not sure it was cancer. lymph nodes can be large for various reasons. i was in this weird purgatory where i did not know whether i had stage 4 or stage 3. my cancer was very slow growing.

we watched it on the c.t. scan for almost one year. the lymph nodes would get a little bigger, a little smaller. it was a yo-yo effect. katie: during that time, you were getting no chemotherapy? >> no chemotherapy, just monitoring. we did not know if i had cancer. psychologically, it was a challenging time. it was almost like purgatory. i did not know which direction to go. i knew if i had stage 4, i would become a fighter and do everything i could to combat it. if i was cured, i wanted to move on with my life. i was kind of stuck in the middle. after a year of monitoring, we had a couple of scans in a row that showed enlargement in the lymph nodes and a couple of spots in my lungs. i was at stage 4. katie: you went back on chemotherapy? >> when you are stage 4, it depends a lot on the patient and the doctor.

there is a lot of leeway. i was not surgically resectable, i use the phrase currently incurable because i look at it like melanoma where people were considered incurable 10 years ago and now are doing fantastically. i was currently incurable at that point. since i had such a low growing -- such a slow growing disease, i was having a good life. why don't i put off chemotherapy for a while and keep monitoring it? my doctor is a fantastic oncologist and agrees with the plan. i went for a year without chemotherapy and monitoring. i went back on chemotherapy where we made a judgment call and had to weigh the quality of life with treatment. i went back on chemotherapy. katie: you have been an extraordinary inspiration to so many people, tom. i know you have been writing a blog called "adventures in living terminally optimistic." you have helped many patients

navigate the clinical trial system which can be quite confusing. why have you done all of that? what has that given you? >> for two different reasons. i started with the blog. i started because when i was first diagnosed, the first thing i did was go to google and find a blog. it gave me a lot of comfort. the blog i went to, i loved it because it was realistic. it talked about cancer in harsh, realistic terms. but it always had hoped involved in it. -- hope involved in it. it brought me so much comfort. i really started the blog because i wanted to keep my family updated. i did not want to bombard people. i wanted to do something where they could look at a blog. originally, it was going to be a private blog. at the last second, i decided to make it public. i imagined a new patient being

diagnosed going to google and needing comfort. i wanted to pay it forward. it became public. i wrote my first blog piece. all of a sudden, what had been planned to be an update to my family turned into so much more. i quickly realized within the first post that i had a very unique viewpoint. i was a scientist so i knew up-to-date information on science approaching clinical trials. i knew a lot about clinical trial data coming out. katie: you could basically translate it. because when you are thrust into this world of cancer, unless you are trained like the three of you and you, tom, it is like suddenly learning a foreign language. >> exactly. i knew this information. i wanted to help other patients. i decided i can write about this in layperson terms.

it then became a real mixture of a blog where i alternate. i go back and forth between personal stories, my own cancer journey in harshly realistic terms. i talk about chemotherapy and vomiting, all of the emotional things, family, young kids. but i alternate with posts that are scientific in layperson terms. it was meant to share with my fellow patient population the things that i knew. why would it be fair for me to know these things and not share it with my good friends? i am friends with these people. i think the two things played off of each other nicely. it was somewhat by design, but it took off more than expected. there are other places to get trial information or scientific information in layperson terms. when a fellow patient reads about it from someone who knows what they are going through who has skin in the game, it makes it so much more powerful. my little blog started taking

off. i now have tens of thousands of hits per post. i am in 140 countries, six languages. my biggest readership is in china, in chinese. everything is translated by a group of scientists where i work who are chinese immigrants. i get so many messages from people. it has been so rewarding. that was the start. i realized there were limits to what a personal blog could do and i started working with a couple of organizations. i became their in-house scientist and i write for them and work with them educating patients in layperson terms through their network basically which is much more than a personal blog can do. we may want to talk about it later. then i started working with the clinic which is basically a private community where we talk

about colorectal cancer trials 365 days a year in a conversational tone. i recruited fellow scientists who have a personal connection to colorectal cancer. we give them information on trials opening up because it is hard to find the information normally. the real purpose is to explain the trials in layperson terms. we have more than one professor of immunology to talk about immunotherapies in this private setting that is facebook-based. it is a private conversation. patients can go to their medical oncologist with trials that they have been made aware of, which is hard to find without help. they have a basic understanding in layperson terms. we also supply pdf's for the oncologist to read. it has been amazing. katie: well, you are amazing for doing all of this and helping so many people while you are going through your own cancer ordeal.

i want to talk about a couple of the things you raised with the folks assembled here. one is, you were 40 years old when you were diagnosed with stage 3c colon cancer. there was a study out recently led by the american cancer society scientists that showed the incidence for colon and rectal cancer is going up for people under the age of 50. of course, 50 is the recommended age for screening unless you are symptomatic as you were. tell us more about the study and what your reaction was to it. >> this is a report from the people who keep score of who gets cancer in the country, where they live, differences between men and women,

differences in ethnic groups. there was a lot of good news in the study. we are finding colorectal cancer mortality broadly has been declining, particularly in folks above the age of 50 who get screened. the people who get colonoscopy and whatnot. there is clearly a benefit. overall, it is getting better. screening rates are going up. survival rates are improving. the worrisome thing, in the same report card, is there is an increase in colorectal cancer incidence and death from cancer in this younger age group. they are not the people typically getting screened because they are younger than 50. i don't think anyone knows for sure the reason, but some of the things we know contribute to colorectal cancer. obesity, dietary habits, and the like. maybe this millennial generation

has more of those risk factors for colon cancer so they are getting it at a slightly younger age. that is worrisome. we need to figure out a way to help. katie: compared to those born in 1950, those born in 1990 have doubled the risk of colon cancer and four times the risk of rectal cancer. the press release with the study said our finding of colorectal cancer risk for millennials has escalated back to the level of those born in the late 1800's. it is very sobering. educational campaigns are needed to alert clinicians and the general public to help reduce delays in diagnosis which are so prevalent in no people, but also to encourage healthier eating -- in young people but also to , encourage healthier eating and more active lifestyle to try to reverse this trend. neil one of the things that came , out of this study was a discussion about the screening recommendations. right now, the american cancer society and other organizations recommend screening start at age 50. some organizations, 45 for african americans who have a slightly higher risk.

do you think the screening age needs to come down for colon cancer and rectal cancer? >> i think studies like this are exceptionally important to focus our attention on the increasing incidence in various age groups. this is the type of data the folks that guide the recommendations for the age of screening will use to make recommendations. studies like this will start the conversation. they will take it one step further and decide on what the screening age should be. that is the one we will follow. there are certain populations with higher risk features that should have screening at lower ages, particularly family history for example. symptoms, as mentioned earlier. those are specific indications. it will overall depend on the analysis of this data. katie: what do you think is behind this increase among younger people? >> that is a very good question. i don't think we know just yet.

the article made the point of healthy lifestyle is important, diet may be important. exercise may be important. there are potentially other factors changing the incidence of colon cancer and rectal cancer in a younger age group. knowing this is becoming a problem will prompt discovery into the cause. we are just at the beginning of answering that question. katie: not to be too graphic, but one of the things i have discussed with doctors about the study is the importance of digital rectal exams. and that many doctors and patients do not want to get those done because they are uncomfortable or whatever. but that is critically important when it comes to diagnosing rectal cancer in particular. >> rectal cancer, you're talking to somebody who was a prostate cancer doctor for a long time so digital examinations are something we use frequently to look at that space. the key is going to be if there is going to be more cancer in this generation heralded by more cancer at a younger age, we need

to get on top of this. we need to figure out the risk factors. can we deploy public health maneuvers to make them better? and then i think we will develop new screening tools. if we can find d.n.a. on a hair follicle at a crime scene, can we find cancer d.n.a. in the circulation or stool or something like that? katie: not nearly as invasive as colonoscopy. >> i think those things are on the horizon. i think they are coming. katie: i am always worried to talk about that because i am afraid that will discourage people from getting screened with the tools available today because they are waiting for something on the horizon. >> i think the topic of screening test is a very emotionally charged topic. there are a lot of invocations of the right age to be screened. nobody wants to be screened at the age they should be.

we have to recognize the downsides of screening in the lower risk population. what could the false positive rates be and the additional cost of testing be? ♪

♪ katie: let's talk about younger patients and melanoma as well because it is really increasing among younger women in particular. what can you tell us about that?

>> melanoma, like most cancers, is a cancer of aging. it tends to happen to people in their 50's and 60's and so on. melanoma is unique in that it is the most common cancer among young women ages 25 to 29. why is that the case? perhaps it is excessive exposure to ultraviolet light. we know if you look at the d.n.a. sequence of melanoma that from sun exposed sites, ultraviolet light exposed sites, you can see the footprints of d.n.a. damage in those melanoma cells. it stands to reason ultraviolet light played a role in causing those melanomas. so why, if you are a young woman, would you jump into a tanning bed where they will bombard you with ultraviolet light? it may well be, although i do not think there is data to support it, that high exposure

to u.v. light is playing a role in this high prevalence in the -- these younger women of , melanomas. that said, i think another factor that could potentially play in is that nobody expects somebody in that age group to have a melanoma. i suspect some of these folks are underdiagnosed before it becomes a terribly aggressive situation. >> that is true in colorectal cancer as well. we talked about screening already. another thing from the study is i was lucky. i had symptoms. i had a good gastroenterologist who immediately ordered a colonoscopy. unfortunately, there are a lot of doctors undereducated. it is possible to get colorectal cancer under 50. katie: 11,000 cases a year. >> i know people who had symptoms for one to two years.

they went to their doctor and were not taken seriously and even asked for colonoscopies and were not given them. i think because of undereducation, that it is possible. katie: i am sure you have heard stories of people who had blood in their stools who were basically told they had hemorrhoids. >> exactly. i hear those stories every day. i think the worst aspect of it is that younger people are diagnosed with cancer but they tend to be diagnosed at later stages because they are not taken as seriously with the symptoms. for younger colorectal cancer patients, they are often diagnosed at stage 3 or four. katie: in my husband's case, it was stage 4. it was all over his liver by the time he was diagnosed.

>> it is linked to survivability rates. those statistics are feeding into that study. katie: what can we tell people watching at home who may have cancer or have a lacuna cancer and they are desperate for information about clinical trials and just cannot find them? they do not understand when they are eligible. >> the key to understanding clinical trials is communication. that communication should be had between patients and their physicians on an ongoing basis. the question could be as simple as, what clinical trials are open? what could be happening? which one should i be following? there are phases one, two, and three. phase one is early trials where we are trying to determine the dose of the drug and the side effects of the drug. a phase two clinical trial is to know the dose and how well the

drug works. that could be part of phase one. a phase three clinical trial is comparing a potential new therapy against a standard of care. let's talk about phase one clinical trials and phase two clinical trials. these are usually small clinical trials. there may be 20 to 40, that is the general size of a clinical trial. they may be open for a few months. they may open at certain times. three patients may be enrolled and then there will be a time when the trial is not enrolling. it is a cumbersome process trying to stay on top of what trials are available. at memorial, the ability to put patients onto clinical trials is of paramount importance to us. it is very important to our patients. what we attempt to do is if a patient is looking for a clinical trial, we will attempt to match up each of our patients with available slots on clinical trials so we can get as many patients onto the most

appropriate clinical trial for them. katie: how do you know if you want to get the standard treatment, the first-line treatment, i think in your case, tom, it has been around since the 1950's, which is maddening to me, or you want to do a more experimental drug? bill, that is a hard decision, right? go with something proven to be potentially effective to something that they do not even know the dosage you should get. how do you wrestle with that? >> i think one of the things that is getting much better about making that decision is you want to be educated and empowered for the treatment of the standard of care and the prospects in a clinical trial. that is why the blog will be helpful to people. if you look back 20 and 30 years

ago, we were discovering anti-cancer drugs by screening things. these were drugs that would kill cancer cells indiscriminately. the only thing we knew for sure is the more we put on the cancer cells, the more we can kill. the clinical trial was how much we could give somebody. could we give somebody enough without hurting them enough that they could kill the cancer cells in the body? this was inefficient. it would take a long time to find the dose. we had no idea which cancer it would work for. is it better than the best we got? if we add it to the best we have got, is it an improvement? tom worked on these inhibitors. think about how differently the clinical trial pathway was designed. they had an idea of what drug they wanted to use for a very specific kind of cancer with a good idea it might work. that was the clinical trial they did much faster, much more

rational. you go back and look at the early phase drug trials 20 and 30 years ago, i think it is probably 5% of everybody who participated benefited. no more than that. now it is totally different. you want to participate in these clinical trials of targeted therapy because the chance to benefit is so much higher. katie: i know this is one of the major goals of the moonshot program that vice president biden was so critical in launching, to make clinical trials more accessible and to educate people about them and get more people to enroll. >> getting people to enroll in clinical trials, getting communication between the physicians running the clinical trials, between the basic researchers doing the work in the lab that are allowing us to identify which trial to take to the clinic. i think it is very important for us to recognize the tremendous investment needed in basic research so we can understand

which clinical trials we should take forward. >> getting people to enroll in clinical trials, getting information between the basic researchers that are doing the work in the lab that are -- what we are trying to do. ideally, we will understand how their immune system may be made stronger and focus on that particular aspect of their immune system or why their immune system is not attacking the tumor. that kind of edification requires a lot of communication. katie: that is a good segue to what is on horizon. you wanted to say something?

>> we are talking about access to clinical trials where people need to ask question and they gain information as you did. one of the access problems that is magnified for clinical trials are some of the health disparities, underrepresented minorities, people with lower incomes, more difficult for them to get back and forth to the treatment center very often. we can allow that to happen. we have to make this clinical trials enterprise available to everybody with cancer, and that is going to take a lot of work. katie: it is interesting, tom. in your experience, i am sure you were searching for clinical trials and finding that the resources available were sorely lacking in terms of giving people information they could truly understand. >> before we move on to the next topic, i am so glad you brought up the 3% to 5% statistic. i don't think clinical trials are necessarily appropriate for

100% of cancer patients. my viewpoint is that 100% of the patient currently incurable should have a discussion with an oncologist. the current statistic is a travesty -- is a travesty, because there are inherent differences in what some treatments can do. in the age of immunotherapies it is a travesty that the system is not more easily accessed for all patient groups to get way beyond that 3% to 5% marker. katie: this is a good segue. we are throwing around a lot of terms that people may be scratching their heads about at home. that is the new cancer research that is really providing a lot of hope for cancer patients. that is programs taking us further to finding a cure, at least managing some of these cancers, like a chronic illness. one is immunotherapy.

we are going to do sort of cancer 101 for people watching at home. an immunotherapy approach is bolstering the body's immune system so it can kill the cancer, correct? they explained this to me earlier. three different types of immunotherapies. can you explain those in layman's terms, bill? >> first the immune system is remarkable. it can recognize a virus that comes in, a bacteria and infection and fight it off. it can recognize your cells, if they are in my body if i had a kidney transplant and reject it. it can also see the differences in cancer cells versus normally -- normal cells. if the immune system can see those differences why did the cancer grow in the first place? can we goose the response of the -- response in such a way that

it eliminates the cancer. katie: to turbocharge it. that is one of the methods being used. that is consistent across all approaches to immunotherapy, correct? >> that is correct. one of them is to take the brakes off the system so it slows down and doesn't harm normal tissues. you take the brakes off for some cancers, the one where the system has mounted a response, traveled to the cancer, and we we both have adolescent girls, and it is the talk to the hand response. katie: and cancer says you are not going to get me. >> and when you thwart that response, the system is unleashed and can eradicate it. immune checkpoint inhibitor therapy. jim alison worked on one of them. there are several of them. we were talking about the proliferation of these types of treatments and working their way into the clinical trials.

>> that is bolstering the immune system and stopping the cancer from getting the immune system from doing its job? >> they are very nefarious, but if you get rid of that, the immune system can destroy it. katie: what are other approaches? >> one is to take the immune cells out of the body and empower them. it's a funny name, they call them car t-cells. you are taking immune cells out of the body, increasing their numbers, re-infusing them and sending them after the cancer. another is using a vaccine approach to instruct the immune system to go after the cancer in the same way as it goes after the measles and mumps and what have you. >> the next set of clinical trials is a combination

immunotherapy. we need to allow it to get in, but we need to make it stronger with a drug that revs up those white blood cells. once they are in, they are going to do their job and attack the tumors. combination immunotherapies or chemotherapy. katie: this is the reason we need so much more research, because we really need to understand the mechanisms that are used by tumors to resist the immune system's attack. when we talk you envision this , one tumor in one place, and that is the foe you are fighting. but in metastatic cancer, they -- you have many tumors and while they are all related, but they are a little bit different from each other because of where they are located. we're funding a body of work at johns-hopkins to study tumors in melanoma patients at autopsy.

so people who were progressing on their immunotherapy but unfortunately died but were willing to donate their bodies to the study, in a fast time to understand what are all the differences among these different tumors across the different sites in these individuals? and through this kind of work, hopefully we will be able to get a large enough quantity of tissue to be able to tease apart what is going wrong. >> it is an interesting phenomenon. we have people who participated in clinical trials, and unfortunately some of them succumb from their cancer, and they are asking us to figure out why did it escape the treatment and how can this help the next people? so we have people asking us to do autopsies when they pass away. it is remarkable. katie: so immunotherapy, i guess, is the most promising new approach to cancer. is that a fair statement? >> well, i think immunotherapy needs to be put into the context

of the entire group we have to fight cancer. so there is a really benefit and role for continued chemotherapies. there are very good team therapies. there is radiation therapies and surgery for certain tumors. immunotherapy is one of the tools we have. the aim right now for most kinds of cancers is not to replace chemotherapy with immunotherapy, but to use immunotherapy in conjunction, either at the same time, combining it with chemotherapy, because chemotherapy -- chemotherapy suppresses part of the immune system, but it suppresses part of the system that fights bacteria, but it can make the immune system recognize the tumor. when a tumor dies, a smart part of the tumor breaks off and it can tell it to go there.

we are doing clinical trials and combining immunotherapy and chemotherapy. is an excitingng area of research, when to give what drug and in what order. what about vaccines, louise? melanoma, there was a lot of buzz about vaccines working in melanoma. i would love to know what drug was used on jimmy carter, which i guess was an immunotherapeutic drug. our vaccines as promising as they once were -- are vaccines as promising as they once were? >> a patient's immune system seems poised to recognize most melanomas that people develop. >> we knew that stimulating the -- we know that from studies back in the 1800s when a mixture was administered of bacteria to ing up theirevv

immune systems. we knew that stimulating the immune system could activate cancer killing. and in the case of vaccines, most people think of vaccines is you get a stick in your arm like you get your measles, mumps, rubella vaccine and you don't get the disease ever. here we are talking about giving somebody something in their arm as a vaccine and asking it to treat a large existing disease. that has proven very, very challenging. however, recently there was an approval in melanoma of something called t-vac, which is a modified cold virus which is injected into accessible tumors, and it appears to stimulate the immune system locally and to improve the outcomes of those patients treated with this particular treatment. now is that really a vaccine? is it a local therapy?

you can start to slice is pretty fine here. but i think there is still some room for improvement with vaccines in melanoma and other cancers. there are a number of trials going on that stimulate the immune system in various ways. ♪

♪ katie: what approach, tom, are

you most excited about as a cancer scientist yourself, you know about all these different approaches, i am sure. not just for colorectal cancer but a lot of different cancers. one of the exciting things in my view is that there is some overlap of approaches. it used to be very original -- organ specific or cancer specific, and now, as i was talking to bill, childhood brain tumors may be treated the same way as non-melanoma skin cancers through this hedge hog pathway and other methods that i learned about. what are some of the things you are excited about? >> there are so many different approaches that there are going to be a plethora of different ways to help patients in the future. i am going to pick out two, but that is not to discount any of the other approaches. the first one is actually vaccines, including a viral type vaccine like t-vac.

it is a two-step process where you are first educating the immune system of what to look for, because it may not know what to look for. then you take the brakes off. it is a two-step combination therapy. melanoma is also the poster child for immunotherapies because it tends to have a lot of mutations. a lot of things will look kind of funny, a lot of things that look different to the immune system. a lot of targets. it tends to have a lot of cells near it or pre-existing to it. it is kind of a perfect storm to facilitate immunotherapies. that is why it is a poster child for a monotherapy like a checkpoint inhibitor. there are a lot of different cancers out there, including colorectal cancer, like i have, it doesn't have those characteristics. it does not have a large amount

of mutations. it's not something you can really impact. but it also doesn't have a lot of immune cells near it for various reasons, that will probably take years to figure out more fully. other than vaccines, another thing i like is i like to compare it to how do you make a type of cancer other than melanoma look more like melanoma? you can't impact the genetics, but can you get it in such a fashion to get the attention, to bring in immune cells in the vicinity. it is very, very complicated. there can be immune cells that activate and attack the cancer. there are immune cells that actually suppress the system. it comes down to a complicated problem with a lot of co-therapies. first getting the attention of the system is going to be key. then you get it to where melanoma is and then you bring in the combination therapies of

clinical trials. katie: and personalized medicine. i used to say cancer is millions of different diseases and millions of different biologies. my body may respond differently to cancer than louise's, tom's, bill's or neil's. are we closer to saying this person has this specific mutation or this specific protein as part of the cancer cell, so we are going to give this person x therapy while we are going to give somebody else y? >> this is the standard of care in melanoma. in melanoma, a routine test done for all patients is to look for a mutation in the gene called braf. about half of melanoma patients have a particular mutation that actually turns that protein on. so it is actually known to be driving the cancer. there are approved, f.d.a.

approved therapies that target that particular mutated protein and things downstream of it. these things work well for melanoma patients, but unfortunately, resistance is quite common to these dreams in -- treatments in those patients. katie: but awe seeing this in -- are we seeing this in other cancers as well? herceptin is it a discovery. certain breast cancers are receptive to that. are we going to see those kinds of characteristics surface in other types of cancer so a specific treatment targeting that mutation can be employed? >> i think you are. and you are going to see them cross different cancer types. some ovarian cancers, particularly those that arise in women with inherited syndromes, the brca type defect. they have a very specific problem that gives them the defective gene for ovarian cancer. but that problem is an achilles

heel for one particular type of drug. this drug works incredibly well when they have that titular -- a small fraction, 4% or 5% of men with prostate cancer are from those kinds of families and have the same defect may have inherited. through with bad prostate cancers and gets also to treatments and is still getting worse, that ends up 15% of them or so may have that same defect, and they will respond to the same treatment that women with ovarian cancer with that defect responded to. katie: i feel like in the past you threw something against the , wall and see what would stick without knowing an individual's particular characteristics or what their cancer may respond to. but that is starting to change? >> i think you are right on

track with that thought. up until now we have identified markers that will in general not be the target of the therapy, but will indicate whether or not there is likely a response. for example, in colon cancers with a mutation, it tells us that a certain type of drug is unlikely to shrink the tumor. these are markers, but it is not the actual target. what we want to do when we identify new treatments for cancer is to identify the changes that we can design a drug to go directly to that point. that is a change in d.n.a. that causes a protein in that cancer, then we want to turn off that protein. this is the realm of targeted therapy. a lot of these therapeutic strategies are in clinical trials right now so we can learn how to do that. and we can learn which genetic change can be targeted,

actionable mutation for d.n.a. mutations. for immunotherapy, it is a whole different idea, because we are not looking at mutations or changes in d.n.a. we are trying to identify which immune cells are turning off these soldiers and these white blood cells that are trying to get into the tumor. katie: i find it so frustrating that progress seems so slow, but cancer is so complicated. having said that, do you feel that we are, at this critical point in cancer research with data and technology and new approaches, and a new understanding of basic biology, that we are going to see more progress made faster for patients like tom? >> i think the answer is yes. i became a genital urinary

oncology in the first wave of them, and the difference in experience between men i took care of in the 1980's and early 1990's and now is stunning. most of the men we take care of, we look at men who died of prostate cancer, most of them had the disease for a long period of time. had suffered at the end of life for a short time. and that was not true before. we have made more progress more than we credit ourselves and everyone around this table will tell you tomorrow is going to be better than today. katie: what advice would you give to patients? what practical advice? it's hard to find out about these things, quickly. >> if you or your loved won -- loved one hears the horrible three words, you have cancer, take charge. ask doctors. go to websites. there are foundations for almost all the cancers. so many people want to help. ask can i participate in a clinical trial. should i, and until you get the

answer you want keep asking. , >> neil? >> have a discussion with your doctor early on. ask him which clinical trials they should be looking out. ask the doctor to call the academic center and ask what is available. katie what if the doctor says i : don't really know. you are going to have to figure that out on your own? >> then ask again. katie or go to another doctor? doctor, it isher a good question. the answer may be there is no trial, but there may be one. ask the question. >> don't be fearful. don't be afraid to ask your doctor these questions. if you offend them then you , probably need another doctor. hopefully you won't offend them, but keep asking those questions and do look for the disease specific foundation whatever in -- and whatever -- in whatever cancer you have been

diagnosed with, because there is a lot of information across different foundations and different sites and blogs that can help point you in the right direction. be forceful is my advice. katie: tom, as somebody who is in the middle of this and learned so much along the way, what would you say? >> first of all, i think they said it beautifully. i agree with everything i have heard. words out of my mouth. be pushy. don't take no for an answer. if you want to do a clinical trial, use resources from other organizations. go see a secretary doctor if you -- go see a second doctor if you need to. if you do get to a major cancer center, don't take no for an answer. it is your life. katie we have said that : hospitals that have nutritionists, social workers and place toss help people and family, who are critically important, but why not have an expert in clinical trials on-site to help people navigate this very confusing system? >> i agree completely. >> i think doctors want to put

patients on clinical trials. as oncologists, we want to give our patients the best therapy, and that includes clinical trials. it is important for doctors to have access to organizations that can common, communication between doctors so we can learn what information there is. we want to help our patients. >> and that is part of the moonshot program with joe biden. people can navigate the system more easily. patient,cognize as a you may need to go to a different center. you may need to travel. that is just not every trial is -- that is because not every trial is offered in every place. i think that is uncomfortable for people who are not feeling well, but that is part of the way good clinical trials can get selected for individuals. >> and the doctor-patient-nurse relationship in the clinical trial setting is wonderfully collaborative. it is the reason we are in this game, because it is wonderful to work with people developing new therapies as their partner. katie: well, i have always said cancer scientists are really the unsung heroes of our society. i truly believe that.

i think that can be said for each and every one of you around this table. thank you for what you do. thank you for what you do for patients. tom, thank you for being a patients and helping other patients. it is quite remark ashley. -- remarkable. >> and thank you for all you do for colorectal cancer and the community. katie: we are, we are working on it. we are going to keep on pushing for you and other patients. nelson, dr. noel neil, dr. louise perkins and dr. tom marsilje, thank you all so much for being here and helping us understand this mystery that is still plaguing us called cancer. i so appreciate it. and thank you all so much for joining us. ♪

♪ jonathan: from new york city to our viewers worldwide, i am jonathan ferro with 30 minutes dedicated to fixed income. this is "bloomberg real yield." ♪ jonathan: coming up, death, taxes, a rate hike all but guaranteed at next week's meeting. how long before the ecb follows suit? another ugly week for treasury bulls. yields at the highest level so far this year. in the face of rising rates and corporate prices, how much longer is the window open to