>> rose: we begin in evening with the lasker prize and we introduce you to lasker laureates, men and women who are scientists and who, through their research, change our lives. we talk with evelyn witkin, stephen elledge and james allison. where will we be in ten years? >> i think we'll be in a situation where, if there's a precision drug that can genetically type a patient's tumors and say this drug's got a good chance of killing a lot of tumor cells, although we know it's not curative, we'll be combining that with these immunotherapies that can make that curative. the wonderful thing about the immune system is once you get t cells, they're with you the rest of your life and if the tumor comes back, they can attack it again and we can give memory to those drugs that normally are just around for hours. >> rose: we conclude this evening with actor richard gere

who has a fascinating new movie out called "time out of mind" about a man homeless. >> it really is a movie i wanted to make but by the end of it i forgot the man was homeless. that wasn't the issue. i was a deeper kind of yearning for a place that i was interested in, a more spiritual, cosmic voyage towards a yearning for place, for connection, for family, for tribe. where is my place where i am valued, where i am precious? >> rose: lasker laureates and richard gere, when we continue. >> rose: funding for "charlie rose" has been provided by: american express. additional funding provided by:

>> and by bloomberg, a provider of multimedia news and information services worldwide. captioning sponsored by rose communications from our studios in new york city, this is charlie rose. >> rose: the lasker awards are among the highest honorsiin science. they recognize individuals from major advances in understanding, treating and preventing disease. lasker laureates have won nobel prizes in the last seven years. evelyn witkin is joining us, ground breaking search on dna that helped shape modern genetics. also stephen elledge of harvard university, he built on witkin's work uncovering dna repair, a mechanism that protects the human genome. pleased to have both at the

table. welcome. >> thank you. >> rose: great to have you here. >> pleasure to be here. >> rose: you will receive the awards tomorrow. >> yes. >> rose: tell me about you and how your career, why this direction? >> i was a graduate student at columbia. in 1943, i read a paper that came out by two scientists and they established in that paper that bacteria have genes like other organisms, and that hadn't been known before. >> rose: in '43, they did not know? >> they did not know bacteria had genes. and i got very excited when i read that paper because it seemed to me that bacteria would be a wonderful material for genetics. >> rose: to study genes. to study genes, because they divide every 20 minutes, and you can hold a billion of them in one little test tube in your hand, and that my advisor, my

professor at columbia, saw i was so excited about the bacterial developments, he suggested that i do my ph.d. dissertation research with e coli instead of fruit flies, and ealso suggested i should go to cold spring harbor for the summer because that's where bacterial genetics was being born, and i could learn to handle e coli and come back to columbia and do my research with e coli. so i went to cold spring harbor, and it was a wonderful place to be at that time. and you could feel the stirrings of the revolution in molecular biology beginning, and there was much excitement about the new developments both in bacteria and in badg -- in bacteriaphageh

exciting genetics coming out of those studies. so i started out by discovering a radiation-resistant mute pt, and it was unexpected and diverted me from my original plan looking to induce mutations with chemicals, and that became the subject of my ph.d. thesis. >> rose: you would induce the mutation by radiation? >> no, i had planned to study radiation-induced mutation, but my first day in cold spring harbor, the very first experiment i did, i discovered a radiation-resistant mutant. >> rose: i see. why was that important? >> well, this was in 1944 and some of the physicists involved in the manhattan project were quite interested. some were in cold spring harbor. a few of the physicists who had worked on the atomic bomb decided that they were disenchanted with what they had brought and switched to working

in biology. >> rose: and their interest and curiosity was in the effect of radiation? >> well, the fact that a single mutation can increase resistance of an organism 100 fold, they knew i didn't know -- i didn't know, but they knew the bomb was coming and the use of the bomb would expose populations to a huge amount of radiation. >> rose: as it did. so the idea that you can have a single gene mutation that greatly increases resistance to radiation was interesting to them. at any rate, i studied that phenomenon. i got my thesis, i got my ph.d. then i started to think about how mutations happen. the first thing -- well, one of the ways that i worked was to start out with strains that require something to grow, like an amino acid or some other

component of their nutrition, and look for mutations that no longer required that growth factor, that was easy to select, because if you just leave out the growth factor, the ones that have lost that requirement will be the only ones who could grow. and, so, that was a system that i used. and the first thing i did -- i was using ultraviolet light as the source of my radiation, and we didn't know yet, but we found out in the '50s -- well, a little bit later than that, in the late '50s that what ultraviolet light does to dna is to fuse or connect two of the dna building blocks that we call bases, and they're normally not connected to each other in the

fact that they get connected stops the recommendation of the dna. the copying enzymes that usually go quickly through dna making a copy, they're stopped by that kind of damage. that's the kind of dna damage that is lethal unless something either repairs it or tolerates it somehow. and what i was trying to -- well, what i did begin to find out was that there was a repair mechanism that i couldn't identify biochemically at this point, but i could see the effect of it. i could see that it was eliminating the mutations very rapidly under certain conditions. and a few years after that, a repair mechanism was identified biochemically. it turned out to be the same ine i had more or less observed in action, and that's called

excision repair. >> rose: so from that discovery about dna repair, what happened between that time and today? what do we know now that's on the course of learning? >> we know there are very many different kinds of repair. i won't describe them all. but i guess what i'm known for, what the prize relates to is work i did that's called the s.o.s. response for my part in discovering the s.o.s. response. the s.o.s. response and the term s.o.s. as used in its usual meaning to have the international distress signal, a bacterial cell that has this kind of ultraviolet damage that stops the copier is in distress. what i learned was something happens in that cell that the damage itself and the stalled

replication generates a signal that turns on a bunch of genes. we didn't know how many, yet we now know it's at least 43 different genes that are in the healthy cells but they don't make the product, they just sit there. >> rose: in the healthy cell. in the healthy cell. but in a damage cell, they get turned on and they make all their protein products and they go into action, and what they do is, in a number of very diverse ways, they help the cell survive. they repair damage. they get the replication going again, and the way they do that, one of the gene products that's induced at that point in the s.o.s. response is another dna copier that isn't stopped by this damage. it's one of the scientists who

worked on it calls it a sloppier copier, and it's not so fes festidious. it gets by the damage by inserting any base in that position, and chances are that it will be a mistake and a mutation if the wrong base is inserted in the dna, that is a mutation. >> rose: and the consequence of all that is for us? >> the consequence is, first of all, we learned that there is the phenomenon of induction of many genes when you have genetic damage and, of course, what happened after we developed this system and described it in detail that steve elledge who is going to speak after me picked up where we left off -- >> rose: saw what you had done. >> he didn't just see what we had done, he took part in what

we were doing. he's about 35 years younger than i am, we're of different generations but have the same interests. he was a graduate student at the same time i was working on the s.o.s. response and he was working on the s.o.s. response in his graduate work. he did valuable work that -- >> rose: let him pick up the story from there. >> okay. >> rose: go ahead. because the way he picked it up will answer your question about what the significance is now he brought ut to the human level. >> rose: congratulations. thank you. >> rose: so you're there as a graduate student. >> right. so i did my ph.d. in graham walker's lab and graham worked on the s.o.s. response and, in fact, i was the person who identified the gene for the sloppier copier. that was my thesis, so i was very familiar with evelyn's work and the whole concept of the s.o.s. response as a graduate student. and then i got my ph.d., and i

went to stanford, and i was going to work on something completely different. i was interested in plants, i was interested in trying to figure out how to m manipulate human genes, also, so i had multiple interests. i was going to follow up on graduate work, i never intended to, always seems like you should do something different. so i started looking for genes that might be involved in letting us manipulate human genes. >> rose: right. something that's very exciting now. and i failed to find that gene that i was looking for but i accidentally cloned another gene, and this other gene that i found turned out to respond to dna damage and recommendation problems. it was a gene involved in making nucleotides to make dna, those are the building blocks. and i realized that, well, you know, at the beginning, you know, there was all this great work in bacteria, but people in

bacteria, you know, sort of didn't work on eukaryotes, the cells that we worked on. it wasn't at all clear that the same pathways would actually be functioning there. >> rose: were they? similar, but different. so it wasn't this take it here and put it over here. what we found was that they had developed a competely orthoginal, sort of different system to sense problems at dna recommendation forks and transmit that into information. so what i discovered were the genes and the pathway in human cells, eventually, starting in yeast, but that actually are scouring your genome looking for problems and when they find the problem they set up a signaling apparatus that's sort of like sending out radio signals to the ambulances that come in to try to deal with these problems. as evelyn had discussed earlier,

u.v. light makes a specific type of damage and there is a specific type of pathway that can snip it out and fill it in like a pothole and move on, excision repair. but if you have a problem that's in the process of duplicating the dna, and that means you're taking the dna apart and copying it, that's a much more severe problem, and when that kind of a problem happens, you need a very sophisticated response. so the response that i found was sort of the equivalent of the response in bacteria which we know existed at the time, and that turns out to alert and activate a lot of different sorts of pathways that result in the survival of the cell. they do a lot of other things, too. for example, you know, since we're working on humans now, we know what the effects of losing these genes are. so if you don't take care of

your genome, you get mutations you get rearrangements and you can get cancer, you can get developmental defects. >> rose: how do you take care of your genome? >> you have a monitoring system. the dna has the ability to sense its own integrity. it has evolved the ability to know when it has a problem. >> rose: a malfunction. a malfunction. and it calls in the troops. some of these troops are very dangerous. some of the enzymes that you don't really want around all the time. so you have to turn them on at the right time in the right place. cells can't see. they have to feel their way around things. so there has to be something that says, okay, there's a problem here i need you guys over here now to fix this, not yesterday or tomorrow, now. and they get through. because the human genome is very, very complex. >> rose: this is all an automatic process in the human body or is it from outside? >> it's an automatic process in the sense that we carry all these genes that have evolved to

sense the presence of dna damage, called the dna damage response and to alert the rest of your body. now, i said earlier that, you know, in terms of human health, some very subtle changes in the pathway can lead to serious developmental disorders. but the you take the pathway altogether, you can't even duplicate a cell. it's that important. every time you duplicate a cell, there are problems. this pathway is always monitoring things, saying, okay, we have to fix this and that, so life itself doesn't exist without this pathway in mammals. the other thing about it in terms of human health, this pathway, if there is too much damage, you make a decision to kill the cell, and that prevents cancer, and it can also cause another process called senescence and that's when the

cells don't die but permanently quit dividing. these cells are controlled by our pathways that we discovered and accumulate as we get older and actually contribute to aging. someone did an experiment where they eliminated the cells from the mouse that was rapidly aging and the mouse did not age. so it's sort of the ying and i can't think sort of thing which is it takes a cell that's been damaged out of the chance of it becoming a cancer cell, but it leaves it there, and that leads to a problem that's involved in inflammation. these cells promote inflammation which is a problem for a lot of aging-related diseases. so that's a pretty great experiment. our pathway helps control that

process. >> rose: what's the future of that? >> well, it's interesting. there have been companies that have sprung up around, trying to understand aging, calico out of google, and i have a paper coming out in "science" in two weeks that describes a new protein, it's the switch that turns on the inflammation itself. >> rose: if you can cut that switch off -- >> that's why we have to ask the question does that stop things. >> rose: if there is something a cell that turns off or turns on inflammation, if we can figure that -- what happens there and can then turn off inflammation -- >> that presumably would help us a lot and we can prevent aging. this is still a theory but that's the theory people are working on now to try to test. if you get rid of the senescence

cells, you're better off in a mouse. isn't done it in a person yet. but if you just turn off the inflammation part, do you get better and that's what we're trying to figure out. are you still going to prevent the aging. that's the theory. we found the switch that does that and we can genetically manipulate that in mice and sphee this is a part of the aging process or not and it's a target we can potentially effect. >> rose: where might all this go? in other words, if we can repair genes, we can edit genes, some people look at that and they say, you know, let's look at this very carefully because what we could do -- you know, what do they mean when they say look at this very carefully? >> well, tinkering with genes is not something we want to do per- promiscuously. >> rose: because? because we haven't got the knowledge to be sure of the consequences. we have to take this very slowly and very carefully and be aware

of the risks. >> rose: and who makes sure we do that? >> i think the field itself. >> rose: self-imposed. yes. i think we have a pretty good record for regulating our own activities. >> in many tech notle that have been -- technologies that have been developed, they're great in the lab. the question is what happens when we start doing it in people and that's where we have to be extremely careful. these tools are not perfect, and, so, they need to be very carefully managed and their consequences have to be looked at. >> rose: thank you and congratulations. >> thank you very much. >> rose: thank you. thank you, charlie. great to be here. >> rose: back in a moment. stay with us. >> rose: joining me now is james allison of the university of texas. he found a lifesaving cancer treatment that harnesses the immune system. glad to have him joining us as one of our lasker award

recipients. congratulations and glad to have you here. >> thank you. >> rose: what is immune therapy. >> using t cells to go after cancer and eliminate it. >> rose: what are t cells. the warrior of the immune system. they can attack cells affected by viruses and kill them and detect tumor cells as well that express things on their surface that are not supposed to be there. >> rose: and what drew you to them? >> well, when i was in college, the t cells had just been discovered and nobody really knew how they worked and that to me was a fascinating thing that you could have these cells that travel all throughout your body and look for things that might hurt you. >> rose: and attack them? and attack them. even though they're things that they'd never seen before. >> rose: yeah. and, so, my first question which i meant to start with really is

what drew you to medical research? >> as a boy growing up in south texas i was always interested in biology. my father was a country doctor. he did house calls. he encouraged me to be inquisitive and supportive. i thought about being a doctor for a while, but i realized from watching my dad and other doctors, that they have to be right all the time. they have to be able to diagnose and treat properly. i figured out early on, if you're a scientist you only have to be right some of the time. if you're wrong, you move on. >> rose: that's right. immunotherapy, i hear this term in terms of lots of cancers. it's real serious. it comes with respect to some of the attacks on brain cancer now in terms of using polio virus. >> yep.

>> rose: is this the coming field in cancer? >> we'll, i would say it is because the immune system can attack all cancers. the drugs i have developed, they unleash the immune system. they don't treat the cancer, they treat the immune system and unleash it to go and attack and conceivably can work against all kinds of cancer. >> rose: and remind me specifically why the lasker people and you're appearing at a conference i'm having later with a group of scientists, when you mention immunotherapy and cancer research your name is at the top of the list for a good reason. but explain to us exactly how you came to discover what you did. >> well, i was interested in understanding how t cells, what turns them on, how it's regulated. >> rose: let me interrupt you. it's a very interesting idea to me, and this is a non-scientific

question, is the idea of cells being turned on and turned off. >> mm-hmm. >> rose: that's a remarkable idea that somehow cells which are all-powerful can be turned on or turned off. >> the immune system, you have to turn them on and you go from -- you've probably got 100 million t cells with different receptors kind of like the ignition switch, they can recognize different things. but when there is an infection or cancer, they've got to multiply very, very fast, so you go from a few dozen to tens of millions in three or four days, but you've got to stop that. >> rose: at some point, you've got to turn it off. >> you've got to turn it off, so that's what my lab and a few others found in the mid 1990s is there is basically the ignition switch which is the angioreceptor and then another molecule, c-28 is the technical name, but like the gas pedal. then another model called c-24

actually stops the immune response. and, so, the way we put this together in cancer is -- >> rose: you have a starter and an ender? >> exactly. and the idea we have is the tumors get big before the immune system kicks in. this program that's going to turn them off starts but the t cells don't have long enough to kill the tumor cells. if we extend the brakes they can keep running till they eliminate the tumor. >> rose: assuming immunotherapy has the potential you think it does, with are we looking attend of cancer? >> i would like to think of that. some canalsers, melanoma, for example, about 22% of patients that get a single round of treatment with the drugs that we developed that unleash the immune system are alive for ten years, they're basically cured,

if you want to look at it that way. 22%. we've got to get that higher. so there is a combination with another drug in the same class where about half the patients respond. it's so new, we don't know how long it's going to last. but our challenge now is to make this work in other types of cancer. >> rose: and where -- which cancer might that be? >> the ones where these drugs are approved and prescribed are lung cancer and melanoma. but when you get to prostate and kidney cancer and brain cancer, they're a little bit harder because they don't have as many antantigens as lung cancer and melanoma. >> rose: taking brain cancer, i'm told some people it works perfectly and they're essentially in remission or the cancer is removed. >> yeah. >> rose: others, it has no effect.

>> yep. >> rose: why is that? we don't really understand that. i wish i had an answer to that, but we don't really understand. in some cases, it's because maybe there aren't t cells in the tumor when we start, or there are multiple checkpoints. you know, antibodies against two, two are in practice now but there are about eight that we know of. >> rose: what else is going on in the world of cancer? >> well, there is what used to be called personalized medicine, now it's called precision medicine where you do genomic sequencing and identify the mutation that causes the cancer. usually it's something that normally would tell a cell to divide only under certain circumstances but it gets locked on, you know. >> rose: explain that. in other words, this is kind of a layman's conversation for me, but what is it that we now believe causes cancer? i realize there are all kinds of outside factors, whether it's smoking or a lot of other

things, but what is it hat happens within the biology of the body? >> well, to maintain the integrity of the body, cells have to know when they should divide or shouldn't divide and basically if they start dividing, you know, proliferating, making more cells, then you get a cancer. so -- >> rose: if they decide -- do they go wayward? >> sometimes they just grow more than they should. >> rose: an accelerated growth. >> and then they ecape where they normally should be and go to other parts of the body and metastasize and that's the really dangerous ones. >> rose: when they metastasize, do they simply go somewhere and multiply, or go somewhere and infect other cells, or what's the process? >> no, they go there and multiply. >> rose: the same bad cells. yeah. >> rose: just go all over the body and start multiplying and

interrupting body functions. >> yeah, right. so there are ways of, in personalized medicine, you find the mutation that's been caused by smoking or too much sunlight or whatever and stop that molecule from telling the cell to grow. the problem is -- >> rose: stop that molecule from telling the cells to grow. >> yeah, you have a drug that inhibits it and won't let it give the signal it gives. but the problem is there is a lot of ways that cancer cells are so unstable genetically that they're accumulate ago lot of mutations and they're multiple ways they can get around any single thing you can throw at them. so the next coming thing is to -- i mean, so that type of therapy works in 90% of the patients that have the leanings that the drugs decide to treat. but the responses are of short duration. they can be in remission for

months. >> rose: but then the multiplier comes back in. >> yes, stop other mutation, whatever. immunotherapy is different, a fraction of the people respond, but once your immune system starts, they can take it out basically. >> rose: in months. for years. >> rose: no, how long does it take the t cells once they get started to take them out? >> weeks to months. >> rose: that's what i thought, weeks to months. you can go in and be on death's door. >> yeah. >> rose: with a certain cancer. >> yep. >> rose: melanoma, for example. >> melanoma. >> rose: and in two months, you're cured of that cancer. >> yes, and you don't ever have to treat it again. >> rose: and never have to be treated again. >> yep. >> rose: can you imagine what that means to somebody? well, you've seen it. >> i've seen it. i've met many people. >> rose: this must be the great joy of what you're doing. >> absolutely. >> rose: people are alive today because of you and your team. >> that's -- well, that's ultimately the reason we do this work. i mean, the initial reason is to

figure things out and be a scientist and figure out how things work, but it's also at least i feel it's important why we're doing this to figure out how to use what we learn to help people, you know, to save lives stew do you have -- what are the tools of your work? >> oh, many. we have instruments that shoot cells through light beams that can measure different cells on the surface. microscopes that can see different cells. use experimental treatments on mice. >> rose: if something works in mice, why may it not work in humans? >> mice are genetically identical -- there are different strains and the tumors we use

are different so we can figure out how to do it, but people aren't like that. people are genetically very different, more complex and the disease is more complex and it's hard sometimes to extrapolate. but having said that, the therapies, the basic principles of the immune system are the same. >> rose: if you had three times as much money for research as you do, what difference would it make? >> it would make a lot of difference in eni believ en-- ig us to study the patients. there are mouse studies but also we need to have clinical studies about what happens in the tumor when we treat people with these agents, and we're beginning to do a lot of that. >> rose: to find out, if the t cell attacks at the moment of trying to destroy the tumor or

change the mutation or whatever, slow it down from growing, shut off the growth mechanism. >> well, it kills it. >> rose: it kells it. there is two or three ways they can kill. >> rose: what are the two or three? >> one is by making molecules like interferon by killing them. other t cells could punch holes in the tumor cell and inject things in them that destroy their dna. third way are cells are coated with antibodies, certain cells would bind to the antibodies and kill them indirectly. >> rose: where will we be in ten years? >> i think we'll be in a situation where if there is a precision drug that you can genetically type a patient's tumors and saying this drug's got a good chance of killing a lot of tumor cells, even though it's not curative, we can

combine that with the immunotherapies to make it cureddive. the wonderful thing about the immune system is once you get t cells, they're with you the rest of your life and if the tumor comes back, they can attack it again and we can give memory to the drugs that are around for just hours. >> rose: can you introduce t cells into the body? >> you can. that's an alternative immunotherapy that's getting popular these days where you isolate t cells from patients and expand the ones you know react with the patient's own tumor cells and put them back. there's a new field where people actually code the genes that encode the receptors that recognize the tumors and you retarget the cells from a patient and make them go kill and it's a very elegant way, it's a little tedious but it could also work. >> rose: what's your goal next? >> to really understand how these therapies are working and

try to make them work in many more kinds of cancer. i think that we know that we could cure a fraction of patients. we just need to raise the percentage of those patients so we could cure and get it outside of just melanoma and lung cancer and other kinds of cancers as well. >> rose: you're a hero. you really are. so are t cells. >> yes. >> rose: thank you, jim. thank you. >> rose: back in a moment. stay with us. >> rose: richard gere is here. he's one of hollywood's most successful and enduring actors. his latest film is called "time out of mind." he plays george hammen, a homeless man living on the streets of new york city. the "new york times" describes the film as an intimate portrait of a man caught between the desire to be left alone and a need for human connection. here is the trailer.

(bell ringing) >> jesus christ! who the hell are you? ♪ >> are you or have you been addicted to any legal or illegal substances? ♪ >> how about family? you got family? ♪ >> normally, a parent takes care

of his kids. ♪ >> you believe in yourself. why do they care? ♪ >> i have had the feeling for the last ten years maybe that i am just one screw louis of an idiot and i'm just not so sure anymore. am i homeless? >> no, no, you're just -- am i homeless? i'm homeless. i don't exist! i don't exist! ♪

>> rose: people say that this is almost for you, in your own mind, a film you have made to act in, that this was what calls on within you things that you want to put on the screen. >> it ended -- actually one of the reviews, i think it was peter travers in rolling stone said it was a miracle. it was a miracle that got made because this is not an easy subject. >> rose: and you had it for what? >> i bought this script -- i lose track -- 12 years ago or something like that and knew there was a movie in here that i wanted to make, and it wasn't obvious in the script what to do with this, but there was just something that i could feel. i was flailing around, trying to describe what i saw in this thing, and i saw a review in the

"new york times" of a book by a homeless guy, cadillac man, and it was called "in the land of lost souls," and i bought the book and read it. i said, well, this is the way to make a movie. this is it. it's not sentimental, it's not dramatulgical in a sense. he's just telling his life as it is. no hard boiled. no editorializing about it. and i found cadillac man who was living on the streets in queens. his approach in his life, i just saw there was a neo--realist movie in here where the neo-realists were the italians just after world war ii and told real stories that were almost documentary in form. the acting was transparent.

the bicycle thief, that's a movie i always admired. ran into an old friend of mine, oren moverman, who had been the co-writer of todd haynes movie about bo bob bob dylan. i ran into him and said i need someone who's comfortable doing this kind of naturallism. he jumped in and ended up directing it. >> rose: tell me more about george hammond. >> this is the irony. i have no interest in his back story. >> rose: none? none. >> rose: only interested in where he is today in his life? >> right now, in the present. >> rose: don't care about why he is there now? >> i think it explains some things, but that's explaining at a certain level i'm not that interested in, in this movie.

it's not what this one's about. i think we all -- there is the illusion we can be explained by our back story, our history. >> rose: what is it you want us to walk away with, then, about hammond today? nothing? >> no, i want to see ourselves. i don't -- one thing i was very happy about when i saw the first rough cut, and one wanted space to do this. i produced the movie and he and i worked together incredibly close on this, finally showed me a rough cut he was happy with, and i was delighted for many reasons. one, it really was a movie that i had wanted to make, but also, by the end of it, i forgot the guy was homeless. that wasn't the issue. it was a deeper kind of yearning for a place that i was interested in, a more spiritual,

cosmic voyage towards, a yearning for place, for connection, for family, for tribe. where is my place where i am valued, where i am precious? >> rose: okay. you perfectly set up this segue into this clip where you talk to another homeless man, george does, talks to another homeless man -- >> ben vereen. >> rose: yes. i think this is the clip. he's asto astonishing in this. >> rose: he plays a character called dixon. >> he may or may not be an actual person. he may be a friend in my mind, but we'll see. >> rose: here it is. $60,000! in his suit! in his socks! you don't get it! the man didn't have to be who he was. he had all the help he needed! he didn't have to be homeless! they told him he wasn't worth

anything. would you say something? anything? do you understand? >> are you the idiot or am i. what? because that is what i have been thinking about. i have been feeling for the last ten years maybe that i am just one stupid loser of an idiot, and i'm just not so sure anymore. am i hom homeless? >> no. am i homeless? i don't know. 've got no home. i'm home less. >> that's not what it's about. i'm homeless. i don't exist. >> what do you mean you don't exist? >> we don't exist! you don't exist. i exist! >> i'm going to prove to you. they think you're a clown! they think we're clowns! we're cartoons!

>> okay, i'm a cartoon. i'm a cartoon. at least i'm animated! >> i am a cartoon! look at me! i am a cartoon! oh, oh, oh, oh! >> charlie asked me who wrote this, it was oren moverman. he was a great writer. >> rose: what an exchange. we played app lot. you have to be opening to what's happening and in flow with it and be in character so that you're alive no matter what's happening. we were shooting with no extras. >> rose: if you had a magic wand, what would you do to change society's attitude about the homeless? >> oh, we have to start from ground zero, and the transition is are we in this alone from our side or are we in it together? that's the basic decision we have to make. do we work with those of us who

are having problems? are they really our responsibility? or are they an annoyance to be avoided? and that's the decision we have to make as a people, as a culture, as a society, as a planet, are we in this together or not? with all the issues going on, and homelessness -- charlie, from my side, i don't see homelessness as a new york story. but you pick up the newspaper today -- north africans syrians, iraqis, migrants, displaced people, people looking for their place in the universe, where can they and their families be safe. >> rose: how can they help their families. >> what can we do about that? how many billionaires are there in the world now? more and more every day. and then we have that kind of madness? no, we have to make a radical rose: then you must be enormously grateful for the pope

we have. >> yeah, of course i am. i mean, he's challenging a lot of the givens. >> rose: and human and in a real way. >> i think the dalai lama, with this pope together, can do extraordinary things. they're each doing amazing things on their own but are coming from the same place. we're all in this together. >> rose: and we all have our part to play. >> we're responsible. nobody else will fix this. we are going to fix this. >> rose: the reason i'm talk about the pope is he's taking in refugees at the vatican. >> i didn't know that. oh, man. >> rose: and he's asked everybody in every country, you know, you owe it to do more than you're doing. >> we owe it to ourselves. >> rose: yeah. this isn't a giveaway. we're really in this all together. when you have that kind of suffering, that suffering is shared on this planet.

it's an illusion to think we're in our own bubble. >> rose: tell me about more about what you came to understand about george other than what we just saw in that dialogue? >> i found -- first of all, the basic story of how we shot this was with very, very long lenses. they were basically two very long lenses. one a 600-millimeter zoom lens and a 900-millimeter. the footprint of the moviemaking, the first shot we did was a master place. the cameras were in starbucks across the street. i was at the cube. you know, the cube, everyone has turned right there. thousands and thousands of people walk by there. well, i was in character, bad haircut and clothes and i came out and stood there on the corner, and i was in character mentally, physically, i was in character. >> rose: and what happened? nobody paid any attention to

me. do you think i could do that as me? >> rose: as richard gere? of course not, no. but i behaved to people's expectation of a homeless guy, a bum on the street, and they could see that for two blocks away and immediately turned off. i could see eventually -- we did a 45-minute take the very first shot of the movie in which no one made eye contact with me because they had already projected all of these negative things on this person standing still on the corner in a place where everyone else is walking, going somewhere. very few cues led to that judgment. >> rose: because nobody can imagine being homeless, first. >> no, you can't, and i think that's really it. i think -- >> rose: you can? yeah, i think people do. i think people subconsciously know how close they are to losing it, how close we all are

to having it all taken away. i don't think anyone is that secure in their lives, especially in these times. you lose a job, the violence -- >> rose: do you feel that? that you're that close? >> actually, i feel mentally i could go. i was feeling that playing this guy on the street. i could feel, i could feel how easy it would be to lose integration, that mentally i could come apart. >> rose: within the fabric of other things. >> the fabric of our reality is very fragile, extremely fragile in all ways. >> rose: describe george's relationship with his daughter. >> they haven't seen each other in some time, okay. and i think there have been attempts for them to a -- at let attempts from his side. the timing has been wrong. he hasn't been in very good

shape and there's a lot of history that hasn't been fixed. >> rose: roll give me those photos like that? >> i didn't have a place to put them. i'm changing places right now. >> what is it you want? you want money? all right. well... here. that's all i have. what else?

>> you seem good. what else do you need? i don't want to get involved in this ever again. i don't. >> all right. stop feeling sorry for yourself. >> rose: we didn't go that far. >> that was an amazing shot. we were just talking as it was playing. almost a whole movie through glass, through windows, through things going by. reflections on the windows that are always moving and dancing.

metaphorically like our brains. our minds are always dancing, even if we're still, this is going on all the time. that's jena malone, one of the best actresses i've ever worked with. this was the first day we shot together. we didn't rehearse a lot. i didn't want to do that and oren didn't want to do that and jong jena dii don't think jena . we were in our characters. i was to happy she was so good and so much fun and so rich. >> rose: are you working all the a time? are you spending a portion of time as you always have in your faith and in your commitment to the dalai lama? >> well, that's a lot of what i do for sure. i mean, he's my teacher, so i'm still learning. you know, i think that's one

of -- your life is still about learning. every time you do this, you don't come into it doing speeches, it's a dialogue of what can i learn here. >> rose: exactly. that's why it stays so fresh. >> it's alive. that's why people want to do this. that's a deeply important part of what i do, and i have been chairman of the board of the international campaign fort fort for 25 years now. movies are actually what i do as a man. my profession, i actually am an actor. ui'm admitting it here for the first time (laughter) it's opening in new york now, opening in l.a. i think just last friday. but we're rolling this out in terms of social action, social change, too. i mean, it's a really important

part of what i want to do with this movie. >> rose: to make for a different attitude in funding programs that connect to the homeless. >> connecting with programs we know that work. housing is number one but it's not the only thing. you have to create community. >> rose: thanks for coming. thank you. >> rose: richard gere, thank you for joining us. see you next time. >> rose: for more about this program and earlier episodes, visit us online at pbs.org and charlierose.com. captioning sponsored by rose communications captioned by media access group at wgbh access.wgbh.org

man: it's like holy mother of comfort food.ion. kastner: throw it down. it's noodle crack. patel: you have to be ready for the heart attack on a platter. crowell: okay, i'm the bacon guy, right? man: oh, i just did a jig every time i dipped into it. man #2: it just completely blew my mind. woman: it felt like i had a mouthful of raw vegetables and dry dough. sbrocco: oh, please. i want the dessert first! [ laughs ] i told him he had to wait.