>> charlie: welcome to the broadcast. we begin this evening talking about science with recipients in the lasker awards one of the most prestigious awards in medicine and science. we talk about stem cells and new developments there with john gurdon and shinya yamanaka. they have been involved in understanding genetic basis of certain cancers and specific drugs that can be used in treatment. our recipients are dr. brian

droorp, nicholas lydon and charles sawyers all involved in gleevek all used in the treatment of leukemia. then we turn to baseball with two legends talking about the essence of the game, hitting and pitching. reggie jackson the great hitter and bob gibson, a great pitcher. a passion for what they do, next.

captioning sponsored by rose communications from our studios in new york city, this is charlie rose. john gurdon and shinya yamanaka. john pioneered the practice of cloning through his experiments on frogs. he is now a professor at cambridge. dr. yamanaka made international head lines in 2007 when he converted an adult skin cell into a stem cell without the use of an embryo. he's at the university of japan. i'm pleased to have both them

both here at this table as they receive the lasker prize in new york. welcome. what's interesting about this your pioneer work was 30 years ago. >> yes. >> charlie: then you had a fuller implication. >> that's right. >> charlie: what did you do. >> i was involved in the early nuclear transif you are experiments as we called them. >> charlie: the new chest of the cell. >> yes you take the new chest of one cell and implant it into an egg having removed the chromosomes from that egg. so the egg has no genetic material of its own but it receives the nucleus from a specialized cell. any other kind of cell. and the outcome is that this combination can develop normally. these experiments such as were explained were done in frogs. so the outcome of that is you

get an adult frog combining the nucleus of a body cell with the egg of the amphibian. you say why should one want to do that. there's a very good reason at that time because we didn't know whether the different cells of the body have the same genes or they don't. >> charlie: now you know that they clearly do. >> i would say we know they clearly do with one rather special exception. excuse me. and that was an important question in the 1950's and 60's. so this kind of experiment was done to try to find out if it was really true, that different cells have the same genes. and the reasoning was that if you could take the nucleus of a cell, like say a skin cell and combine it with an egg and get a

normal animal, in this case a frog, then that must mean that the skin cell had all the genes necessary to make the complete animal. that was essential the results obtained after certain number of years work. and i think that led to the view we now hold that all the cells of the body have the same genes. >> charlie: you had instantly the idea of the possibilities positive and negative for cloning and working out all the things that were necessary to further the scientific progress, which is creating tissue and everything else. >> let me comment on that. when these experiments were first done, there was no intention of creating a clone. that was the in one's mind at all. cloning is a bi-product. if you have an unfeather liesed egg and you grow an animal that

answers the fundamental question of the conservation of the genome as we call it. the clone was a by product of that because if you do this several times over, starting with the same kinds of cells, you get a large number of genetically identical individuals. like twin, identical twins but you might get 30 or 40 of them. and that's nowadays called a clone. that wasn't the purpose of the experiment. as a matter of fact, it didn't have any very particular importance as such. i don't think it does still. >> charlie: then comes you. >> yes. >> charlie: tell me what you do. >> okay. so we succeeded in combining skin cells back to stem cells. >> charlie: you take somebody's skin yells. >> yes. >> charlie: and you can recreate the kinds of original stem cells that created the tissue which created the organ which created the person. >> yes. all stem cells are very similar

to so-called embryonic stem cells. they can proliferate rapidly and make any kinds of cell in the human body. so they are very very useful. however, we have to use human embryos to identify the cells. so many people are against the usage of es cells, embryonic stem cells. so we are working at big programming more than 40 years ago, he showed that es cells and skin cells, although they are different, they look different, their functions are totally different, but he showed that skin cells and es cells have exactly the same grouping for cells. the grouping is a set of genes.

and he showed skin cells and es cells are the same in term of blue print. >> charlie: then you did what. >> so we identified very small number of factors. namely only four factors that can convert skin cells into es-like stem cells. so all we have to do is just to put those four factors into skin cells, and after a must not, they become es-like stem cells. and we named those stem cells ip cells to reproduce important stem cells. >> charlie: you both know, the controversy has been much discussed in terms of embryonic stem cells and this is not the program to do that. we've done that program a number of times before. what's exciting to all of us is the possibilities of what you both in terms of the combinations of what you have

done, in terms of taking a stem cell, whether it's embryonic and then going the other direction. where are we in that? and what is the frontier for that? >> so with this new technology, we can do at least two different things. the first one is kind of in vitro application. so we can make stem cells from any patients, all we need is small skin biopsy. then we can make ipf cells, stem cells. then we can make heart cells or muscle cells or neuro cells. so those cells have the same grouping with the patient. so then we can use those heart cells or muscle cells or neuro cells. >> charlie: go ahead. what's fascinating to all of us and i'm trying to simplify a very complicated process. what's fascinating when you take

the adult cell, you can take it back and make a stem cell and then create cells for, as you said, muscle or skin. how does it work create muscle and some create ... >> so we have to instruct skin cells. we have to ad growth factors or cytokines to combine cells into any type of cells like heart cells. we've done a lot from development, human development. >> charlie: how much do we understand about the process of going from the stem cell to the rest of the journey. and how much you can -- go ahead. >> this is still ongoing. we don't know 100%. but we have new cells from ef or ipf cells very effectively and we can also make heart cells

very effectively from ec or ipf cells. >> charlie: but we're a long way, are we not, from being able to know how to do that and being able to know how to get it to, let's assume in an adult, the process of getting it to, if you have damaged heart cells, to replace them with healthy stem cells that you created. that portion, that injection into the heart and locating the right place and connecting it to the old tissue is the difficult one. >> yes. so many researchers all over the world are now working very hard on those aspects. but you know, because ipf cells we don't have to use human embryos. so i think that will speed up everything. hopefully in the very near future we can come up with a new

way to differentiate ipf cells to any types of cells. >> charlie: so therefore this eliminates the debate about embryonic stem cells because you no longer need them. >> yes, we still them. >> charlie: you will continue to need embryonic stem cells. >> yes. >> charlie: what is your quest about. >> what i want to achieve from my life or the rest of it is that what you mean. >> charlie: yes. >> people often say why don't you retire and live on your laurels such as they may be but actually there is a question, and i connect plain it this way. because when i mentioned earlier that the nucleus of a specialized cell is combined with an egg to make a new organizism, something pretty substantial has to happen to that nucleus has has to under undergo that change.

the question arises what is it in the egg that is doing that. and this is a pretty remarkable characteristic of eggs. other cells can't do that. so there's something special inside eggs which can reprogram a nucleus, make it almost go back in its life history and start again. and i think it would be extremely interesting to know what those components are and how they work. >> charlie: what are my choices? >> you mean what are the possibilities? >> charlie: yes. >> well, there are a number of ideas, but perhaps the most likely one is that there are special molecules in the egg which have a way of uncovering the genes that have become shut off in development. so when you make, for example a skin cell, the genes needed for brain or heart and other things are shut down. they're not in use anymore. but when you do this kind of reprogramming experiment, you have to reactivate those genes,

remove the components which shut them down. so the one option, one idea you can have is that the egg has special components that can remove these represses as they might be called, which cover up unused genes and open up again for further use when the reprogramming takes place. and the problem is to find out what these are. so that's, i would say, as such time as is left to me, i would love to now how that works and what these are. you might even say why would that be useful. actually it might, inspite of the brilliant work of dr. yamanaka, i think if we knew how an egg can reprogram the nucleus without any added genes, this could actually be quite useful. and could, for example, enhance the efficiency with which your procedures work. >> charlie: are you interested in this question as well. >> yes, very much. so the efficientity

[indiscernible] compared to reprogramming of our eggs. so we assume it's something, something very important. so that's what i really want to find out in the rest of my life. >> charlie: if i take all the lasker award recipients, scientists engaged in discovery passionate about finding answers, what would they have in common. >> so one possible idea is this, that they might be people not so inclined to follow the traditional route. you join a lab and the lab is doing all these kinds of things it does and you become a graduate student, post doc and you follow along those lines. it may well be the people who recorded these particular recognitions, the ones who like to diverge from that path, that road and take a different route, find something unexpected. i will say to my colleagues, if

we do -- we plan an experiment for you and it comes the wrong way around that might be more interesting. >> charlie: great discoveries in time have been made that way, right. >> sltly right. so this is one possible thing you might find these various people have in common. >> charlie: what would you add to that? >> i think probably one of the common things among is they do not believe in textbooks. >> charlie: do not believe in textbooks. >> yes. i think that's very important. when i was much younger, i tended to be in textbook. that was my biggest failure. >> charlie: explain that more to me. >> well, we tend to believe that everything, which is written in

textbook are true, right. >> charlie: if it's in the textbook, it must be true. >> most of them, many of them. but some of them can be totally wrong. and this is our job to find out what is wrong in the textbooks. so that's the case for dr. gurdon and many people. he did experiments in 1962 when i was born. >> charlie: in 1962. >> yes. 47 years ago. at that time many people do think, do think, did think that eggs and skin cells are different, totally different so many genes have been lost in skins so we cannot convert our skin cells back to eggs. that, i do not believe in that

textbook-type thing. that's why he initiated his own project and he succeeded. i started my own project, many people told me i shouldn't do this, i would fail. but i did not trust in textbook and i did not trust in what other people told me. >> charlie: that's another quality, isn't it when other people say you can't do this, do it. >> absolutely right. >> charlie: so what's the question that you most want to be answer? equivalent to understanding the mechanism of the egg to be able -- >> so the biggest question for meese the molecular mechanism of ipf cell examination. at the moment we've done almost nothing about how and why those forefactors can conduct skin cells into the embryonic state. so that's the question i bring them to ask in the next 10, 20

years. >> charlie: that's the question you want answered in the next 10 or 20 years. >> yes. >> charlie: come back and let us know. >> yes. >> charlie: thank you,. >> thank you. >> charlie: thank you for joining us. back in a moment. >> charlie: we want to turn our look this evening at cancer, upon its release in 2001 the drug gleevec was haled as a major advance. it offered successful treatments for patients with a fatal cancer called chronic myeloid leukemia. it may provide a blue print for a generation of more effective -- joining me is dr. brian druker of the organize health and science university dr. nicholas lydon and dr. charles sawyers of the sloan-kettering cancer center. they're all here in new york to receive the prestige lasker award. it is one of the highest honors

in all of medicine, and i'm appropriately thankful that they come to this table to talk about the implications of what they have learned and what they have done. welcome. >> thank you. >> thank you. >> charlie: tell me about what is significant about gleevec. >> what gleevec is done it's taken chronic myeloid leukemia with a life expectancy of three to five years and turned it into a manageable disease with a life expectancy which we assume will be normal. and it's done that because we understood precisely what drove the gloat of that leukemia and we developed a drug to shut down that abnormality, kill the cancer cells without harming normal cells. by doing that we generated an effective non-toxic pill that people take once a day that turns their cancer into a manageable condition. for the future, we need to develop many more drugs. we already have dozens of drugs

like gleevec on the market, and hundreds down the clinical trials following that same paradigm. understand it and you can fix it. that's the genomic revolution those occurring right now in cancer. >> charlie: how did you come to understand it? >> 20 years ago we had a war on cancer understanding biology. that together with the genome project hat allowed us to know all the words in the dictionary has allowed to accelerate the pace we've discovered in driver mutations now that cause cancer. so cml or chronic myeloid leukemia is driven by one mutation. that one was known actually almost 40 years ago. now the pace at which we can do this with new genomic technologies is months to years

in terms of deciphering the ingredients of the cancer and figuring out where in the wiring diagram we want to make a drug against. >> charlie: how did you find that? >> when we started this project back in, it's about 86, there were very few known inhibitors proate kinases, about a handful. for a short period of time the genomic explosion has shown over 500 of these enzymes. and the enzyme involved in cml was a member of this large class. so what we had to do is, it's almost akin to finding a key that fits a lock in a large build is like this. there are many doors with many many keys, so we have to sit

through many different chemical classes to find compounds that fitted the lock and then using chemistry, evolve these to be relatively selective of that one target so they don't open the other doors or inhibit the other enzyme which is very important for other thing in the body. >> charlie: how did you find the drug. >> that was the next contribution. he and i worked together over quite a long period of time. my lab provided some reagents or tools to his company. one of the remarkable thing was that cooperation between an academic laboratory and the drug companies. and academics identified this target, his group that a drug company took up identifying a drug which they do very well, bringing a drug, and in my lab tested all the models we had developed to validate the initial target, what drove the growth of this leukemia. and then together we brought

charles input planning the implementation of the trials. >> charlie: every single patient showed what manifestation. >> if you look at a patient with this leukemia, chronic myeloid leukemia, the white blood count normally was known to be 5-10,000. there are white counts between 20-500,000. so two to 50 times normal. our patients when they started on this drug had blood counts that range anywhere from 20,000 to 100,000 or more. within three weeks, most of the white counts returned to normal and within six weeks every single one of them completely normal. these are patients who had failed every other therapy has been told buy other doctors, get your affairs in order, you have months maybe a year to live if you're lucky. many of charles patients, my patients, ten years later on gleevec doing just fine. >> so what we learned from this

is some insight in terms of treating cancer through the genetic basis of the mutated cell. >> correct. this is really the first clear example where -- let me back up. cancer cells are complicated. they have many mutations. you can make a drug maybe against one mutation, but what's is the chance that's really going to work. the tumor's going to outsmart that drug. what's remarkable in this case that didn't happen. we used the term addiction. the tumors are addicted to these mutations which we call oncogenes. and so you can, if you understand the wiring well enough, you can identify, for lack of a better word the

achilles heel in which this theme has been played out we come at it with other drugs. >> charlie: what is the cancer that this theme is being played out. >> the two which are most exciting is lung cancer which everyone understands is a fatal illness. there are roughly 10 to 15% of patients can lung cancer in the yachts and you're. there's a again that calls cml and another drug that inhibits that protein which is called terciva and we have patients coming in with lung cancer to find out if they have that mutation or not. if they do they go on terciva. >> charlie: is this cooperation at some level from big or little and research. tell me more about that in terms of how that process may open up

new opportunities. >> i think from my work, it was critical because when you look at these projects of pharmaceutical companies, there's not a human amount of intellectual power on that. from all the things you need to put together. so you need to bring in expertise that you don't have. so let's take a project the way i met brian was i started collaborating with the dana farber institute and this was to bring technology where we could express these enzymes, large panels of them for testing. and you know, without that exchange between leading edge research and academia and application of it in industry, it's very hard to build all this yourself. this is vast amounts of experiments that need to put to

bear for these applied projects. >> charlie: the third part of this equation is government. >> yes. >> charlie: government approval. >> yes. >> charlie: how does that come in. >> it's a shining example how government can work. it was the fastest fda approval the drug on record from the time -- >> charlie: four years, how many years. >> it was three years, less than three years from the initial patient on a clinical trial to approval. but the package that was sent was from february of 2001 to may 2001. 11 weeks in review. most drugs will take anywhere from six months to a year under review before the fda will approve them or not. so 11 weeks. and it was an unprecedented announcement by then tommy tomson been and several other dignitaries, the head of nci was there as well, talking about how the fda can work when you

present them with drugs that work well. >> and some regulations the fda put in place like accelerated approval, which really worked for this drug. >> the third point there is the science that explained why it was working was so solid that it was a completely convincing story. >> charlie: so therefore they're willing to put it on a fast track, they're willing to -- >> not only could we understand why it was working, we could understand why it stopped working in certain patients. so the science underlying this makes so much sense that the data was completely convincing. >> charlie: give me the landscape of cancer. today we're talking about genetic mutation. >> we're talking about a theme matching the right patient with the right drug. we're talking about instead of taking your car to a mechanic and not having a clue what's broken, having them lift up the hood, look at the engine and figure out what's part's broken and replace the broken part and fix your car.

we're talking about looking inside of a cancer cell, figuring what's driving the growth of it. yes it growing and growing and growing to cause that tumor in shutting down that part specifically. the results with this inhibitor in melanoma, gleevec-like results. there's 10, 15% of lung cancer patients who are just starting to see that we're turning the tied against cancer with this new paradigm. we're moving from an era of non-specific chemotherapy to very prehe'sly targeted drugs that are more effective and less toxic. >> charlie: that's the story. >> that's the real story on gleevec. >> charlie: what's the big unanswered question about cancer? >> one is why do cells get it in the first place. why do i get a mutation and you not. we know -- >> charlie: what are possible answers for that. >> we know that certain environmental exposures, smoking, obviously, exposure to chemotherapy for breast cancer can cause a patient to get

leukemia later. damaging the dna in blood cells. but we don't know why most measures don't have these exposures. it could be just aging. cells as they divide and get older, it happens in copying the dna and mutation is created. if it's in the wrong cell that's probably what happens. >> charlie: go ahead. >> now charlie's absolutely right. it's absolutely clear that the number of the people get cancer increase with age. that's absolutely clear. what's becoming even more clear is that some of the programs that are set very early on, even at birth may predispose this and there being certain genetic abnormalities. we know for example the warner to exposessed to breast cancer. some are in their 30's and 40's.

there are other similar sorts of change that may predispose men or women in cancer later in life. again in this genomic revolution we're going to begin to understand that. if they think beyond targeted therapies to prevention, we'll actually get to an area of targeted prevention where we under what somebody's individual genetic risks are to develop cancer and they should be able to target those. that may be 30 to 50 years later but that revolution is coming. we can see hints of that already. >> charlie: so the more everybody has some mapping of their own personal genome and developments called collateral development may very welcome the a time in which you know that you have a jaw theyic predisposition to some kind of cancer. you can begin to think this in terms of prevention by being able to target a particular drug, a particular treatment. >> that's exactly right. >> charlie: so we look forward in this century to the

what? >> i firmly believe that we'll be able to look forward to that in this century. >> charlie: are you looking forward to the ratification of death from cancer. >> probably not entirely. and the analogy i've used is to infectio disease. if you look back a hundred years, life expectancy in this country was 47 years. now we're in the mid 70's. most of those have come from eradication of treatability of infection. and that's been with antibiotics, that's been with public health measures and vaccinations. but we still deal with infections. hiv has reared. we now have concerns about swine flu. we haven't eradicated infection but they're not the deadly disease they were a century ago. this century will do the same thing for cancer. >> charlie: thank you. congratulations to each of you. >> thank you. >> thank you very much. >> charlie: back in a moment. stay with us.

>> charlie: bob gibson and reggie jackson are here. they're two of baseball's all time great. both are known for their intimidating presents and poise under extreme pressure. they are mvp's. jackson's five home runs in the 1977 world series pass orlt yankee fork lower. gibson is widely considered one of the great accomplishments in sports history. together they have written 60 feet six inches a hall of fame pitcher and hitter talk about how the game is plays of played. i'm pleased to have them both back at this table. how did this come about? whose idea was this? >> actually, it was they contacted me and asked me if i was interested in doing a book and at the time we didn't know what we were going to do.

and i said yes. we came up with this idea, double day came up with the idea, i'd like to do something with a hitter and a pitcher. who would you consider. and we have several names of different people. we didn't have reggie's name on there. i said how about reggie jackson. oh, you couldn't get him. i said oh yes i can. so i called him reggie i'm going to do this book and he says i'm in. and that's the way it went. >> charlie: you only hit against him in an all stars game and what happened. >> well that's a pretty good story. >> charlie: i know. >> there was a time before that, and i'll let bob tell you that story about in 19. 6 9 -- i'll let him tell that story. the all-star game was in atlanta

and there was always a press conference before that, and bob had pitched on sunday. and he was going, he was announced that he was going to pitch on tuesday and he wasn't happy about it. he had wanted to, his focus was on winning. and doing things for the team. ladies and gentlemen, i pitched on sunday, i should have a couple days off because when we start again on wednesday i'm probably going to pitch again or maybe my turn is thursday. tuesday's too quick. he wasn't happy about it. and so we all knew bob and his reputation and he always had an intimidating factor going with him. he threw high 90's and inside. if you moved you wouldn't get hit. he said i wasn't throwing at him he moved into the ball. first time up i get a double. he hangs a slide i hit it off to right center field and i round second base and i easily turn --

i slowly turn this way and look out under the bill of my cap and he's looking either out at me or the score board or something where the ball hit. and i immediately just turned around like that and looked away from him. >> charlie: why did you do that. >> i didn't want to get punished. i didn't want to walk into one of those pitches the next time i was coming up. >> charlie: is that what would have happened. he looked at you in a wrong way like i got you, you can't -- >> in an all-star game there's a pretty good chance i wouldn't have faced him again anyway. but you never know. i may have seen him in a world series or some other time then. i don't forget things. >> charlie: so everybody that got hit by you, you intentionally meant to hit them. >> no. i would venture to say that probably 70% of the gay that -- guy that i hit i wasn't throwing. >> charlie: so 30% you were. >> i had to protect them. they would knock some goes down and hit them. if i was pitching somebody was going to get it, it was just

that simple. a lot of times when you pitch inside, you throw the ball hard and you pitch inside, you're going to hit guys without really trying, you know. i can say that i never missed anybody i was throwing at. [laughter] >> charlie: so when reggie told you, what did he say to you about, you know, if you hit me. >> no, you didn't say anything about hitting anybody. he came up to me and he says i'm reggie jackson. i said yes, i know you, i'm bob. he says i understand you like to pitch inside. i said yes i pitch inside a lot. he says well if you ever pitch inside to me i'll come out and get you. i said well we'll just roll in the dirt, won't we. he just laughed and walked away. >> charlie: i think i asked you that before but where does that come from. >> i guess i was born with it. >> charlie: really. >> yes. i told reggie when we had a real

conversation a couple weeks ago. i had a brother josh. and josh was mean. >> charlie: josh was mean. >> you talk about intimidation, he intimidated me. at one time i was playing short stop and the game hadn't started but i was going to be the short stop and we were in somewhere in kansas playing on a little field and the whole thing. he hit me a hard ball, i picked it up and threw it to first and it bounced up and hit me in the eye. blood was going over where. josh came out and said let me look at it. he called a guy over with a band-aid, put it on there and said go on back out. here we go again. i was about 12 years old, i wanted to cry and go home. but he kind of made me tough because he expected like most people, they expect affection with everyone and themselves.

he expected perfection out of me and he wanted me to be better than everybody else out there. and he wouldn't accept anything less. >> charlie: so it grew inside of you. >> it did, it did. >> tell -- >> charlie: tell me what we don't know about pitching. >> people think they know a lot about the game. there's a lot more thinking going on between the hitter and the pitcher than people realize. they think the guy throws real hard and he just goes in and gets guys out or the guy's a pretty good hitter and he just swings when he's lucky. no. there's a lot of thinking and a lot of cat and mouse going on. when you're in the game for any length of time, you know, the young kids don't really understand that because you have to be in there and you have to get embarrassed a couple times before you really learn how to pitch. but it's like a chess game.

i may pitch to him one time and next time i may not. depends on the situation, who is hitting behind him. so there's a lot of thinking people don't realize is going on out there. >> charlie: tell me what you think about when you're at bat and you're facing somebody as good as gibson. >> well, the first time you'd face him, you'd try to figure out his reputation and what he does on the mound. after you face him for four or five times, three four times and in the major leagues, bobby had a career of 16, 17 years. >> 17 years. >> and i had a career at 20. so if we're in the same league, after it's all over, i'm going to have 150 more, maybe 200 bats against him. and i'm going to understand his successes and understand where he goes. at the same time in certain situations, he is going to go to his bread and butter, what he likes the best. and that's against me, it would be a fast ball away or it would

be a slide in. he threw what they called a curve ball in between a curve ball and a slide. we called it a hard slurve, in between, a hard pitch. in certain situations, you could look for certain things. he would know what he was going to throw me, i would know what he's going to throw me and it would get to a point to where maybe the game's on the line, he doesn't have any place to put me, say okay i'm coming after you. and those times you do have that, you know, david and goliath battle, if you will. if you have your time in the game like he and i both have, you pretty much know what's going to happen when we go after each other. he may go away and not pitch to me. he may try to pitch on me and touch the corner or something like that. but if he found a hole, a place where he could get me out, if you will, he would stay on it until i hit it.

it may be in, it may be a slider. for me i ran up against a hard slider. like pitching to a left hand hitter. >> charlie: what was your sweep. >> away from me. >> charlie: high or low. >> it didn't matter as long as it gets away. if it gets down too low it's hard to get out of the ballpark. i wanted the ball away from me and you couldn't throw it hard enough. i was in a situation where his bread and butter is away and he's going to come there and pull his hat down and touch high 90's and say all right my friend if you can hit it, go ahead because here it is. >> charlie: what was it that made you mr. october? >> you know, i've been asking some people, in fact i talked to bob about this just a couple weeks ago, i think there's, the common thread is some kind of dna that runs through people

that makes them get the job done. i think it happens at a young age in a person. i know for me it was my father that look reggie i don't want any excuses, i want you to get the trash taken outside. don't tell me it was raining or too cold, don't tell me it was snowing, get it done. and so i took that same attitude toward sports when i got into it and i got that from my dad in talking to bob, something happened to him at a young age, with his brother, it was a no excuse, i don't want to hear anything, get it done is the way my dad talked to me about it. and bob had his version from the his brother josh. >> charlie: what's always been said about you is this sort of brooding. do you accept that. >> no. >> charlie: okay. second thing that's always been said about you is intimidation. >> intimidation comes from the outside. it comes within. the last thing i was trying to

do was intimidate people. first of all, i look like i look and people see me, what are you mad about. well i wasn't mad until now, you know. it's just the way i look. and so people think that i look mean. okay, that's good. many but i got accused of staring a hitter down. in truth i wore glasses off the field. i had a hard time seeing the signs and things. the last thing in my mind was to intimidate somebody but the hitter comes up there and automatically he sees i'm trying to intimidate him or whatever. that's the way i see it. >> charlie: do you think it worked for you. >> well it worked but it didn't work for me but i didn't know. if i had known i would have been nastier, yes. >> charlie: if someone would come out and say bob, it's time to go i think we need to make a

change here; would you accept that. >> i had to. >> charlie: when he said it's time to go, you would go. >> yes. if he says how do you feel, if he says how do you feel, what do you mean, are you still throwing good. well, who is in the bullpen. we got so and so down there, i'm fine. >> charlie: rather than have somebody come in and say i'm fine. >> yes. >> charlie: what if mccotterer comes out and said you're not getting the signal c. >> tim's a funny guy. tim would tell me a lot of thing that i already knew. you know. there's a man on first, you know, give me a shot at him. and i would laugh and i'd say tim, you're not going to throw him out anyway and i'm not wasting any pitches and he would curse at me. one time we had a man on first and third. and there were they outs.

and tim came out and says max is covering second base and he says we're going to go for two. i said no we're not. if a bottom is coming at me i'm going home. he says early in the game you can't play like that. i said i'm playing like that gauze you score one or two a game and i'm not giving up an extra run. so if it comes back to me look for it. and he's storm off. >> charlie: all right roll tape. this is the conversation with tim. what's the worse thing he ever said to you. >> i guess the line was what are you doing out here. get on back behind the plate. the only thinking you know about pitching is that it's hard to hit. barney schultz story. he was a knuckle ball pitcher. he hated going out to the mound with gibson there because bob would say barney, you threw a knuckle ball. i throw fast balls. i don't throw a knuckle ball so how can you help me.

one night in philadelphia, in the second inning, a rare gibson start, he had given opposition or seven earned runs through one and two, right, right. and red sent barney up to take gibson out of the game. and barney, it was an interminable time. i was playing first that night, ted was the kitcher, we're all waiting for the fireworks. barney got to the edge and bob said barney, where have you been. i had been getting hit up out here and you've been sitting in the background. a competitor, most difficult friend. >> charlie: most difficult friend. >> most difficult friend. >> charlie: why a difficult friend. >> because most people are not willing to go through what bob gibson, what he put you through to ultimately become his friend. once you get to that level, then you're happy you went through it. >> charlie: what does he put

you through. >> the same stuff that he put barney schultz through and i had a very difficult time with bob. >> charlie: was that broke through or over time you made a difference. >> i think over time, over time. >> charlie: you had to earn your friendships. >> i think that's the way people are. you don't accept people for face value, you have to get to know them. i have been all my life kind of stand offish as far as making friends is concerned and it takes a while. i think that's the way it should be. >> charlie: we'll talk about hitting and managing. calculated anticipation. what is that? >> guessing. i said that one time on tv to joe garragio and he said oh no,

i don't think lawyer here. i think a lot of people do it, pitchers do it, we do it as hitters. where a guy is pitching you in, pitching you in, pitching you in all the time. and i hit a couple bullets. a ball inside, okay. i come back the next time up, i hit a ball over the fence off a pitch inside. now, with fairly easy analytical thinking, we could call that calculating that i am now going to anticipate something being away from me. and something soft. so i would take the experience that i have as, you know against a certain pitcher and i could take a pitch away from them. i hit two home runs off a slider that's away or down period, a good one or bad one. i'm not going to see that for a while. so even if i see any at bat charlie and it's a ball, i feel as though i've taken that from

him at least for the next few at bats and i'm going to get something hard, i'm going to get a fast ball. so that's a fancy term. >> charlie: yes. [laughter] >> charlie: but informed guessing, informed. you take that. >> informed, right. >> charlie: in 68, it was 1.12 or something like that. >> yes. >> charlie: since then what's the closest anybody's come to your record, do younow? >> i don't. >> charlie: anything below. >> well there have been some 1's. >> charlie: really. >> beginly was a 174. cofax had some 1's and i know

vita 174 and gidry was 178. >> charlie: who was the best player you ever saw. >> mays. mays for us, i don't know for bobby but for me we could watch him like jordan we played against him in spring training. one, you wound up realizing that you were watching willie the way he ran, caught the ball the way he through it in. everything he did had a style to it. and he did everything super. not well, he did it all super. he stole a base stole it when he needed it, threw great, ran great, hit well, hit homers. and was exciting. >> charlie: tell me how sad you are, what damage has been done by all the disclosures to the game you love. >> oh gosh. i think when i first heard about steroids, charlie, i remember not first but maybe after a year

or so and i saw a wreckage tumbling, i went six all time home runs to 13th. in 140 years i was 6th when i wound up playing my career was over. and in the next 140 weeks, i was 13th. and i was talking to many so guys playing golf in vegas and almost got tears in my eyes. i had to hold them back because i love the game so much and admired the path that players like bob and aaron and mays and clementy and root, ted williams. the numbers that they put up were goals that i hope to become a part of. i hope to get approval from the greats of the past that, you know, reggie's a great player. reggie's a good player. and if you got that approval,

then it really meant something because the game of baseball was, has been built on, you know, are our icons and our idols of american history and our great sport of baseball. steroids came about and players ran by some of the greats in the past so fast that i lost understanding of what was good, what was great, what was the best. it didn't make much sense, so i've been hurt by the steroids, if that makes sense. i've been emotionally hurt and bothered by it. i almost feel like it makes some of the players that earned their strikes if you will before steroids. i think like it raises our level of esteem or our stature. i'm hurt by it because i think for some reason it steals from the game. there's an unfairness to it. there's something inequitable

about it and i don't like it. >> charlie: someone told me a story that ted williams and joe demaggio were waiting to see president bush 41 at the time and they had an hour and-a-half because the president was delayed and this person witnessing that conversation said it was one of the great moments in his life to sit there and hear these two giants talk about the game they love. everything from bat size to some of the things we're talking about. what makes a great hitter and what kind of pitches were best for you. some of that same thing or a lot of that and more is here because it comes from two greats but one is a pitcher and one a great pitcher, one's a great hitter. the title is 60 feet circumstance inches hall of fame pitcher talks about how the game is played. i thank you. great to see you. >> thanks for having us. >> charlie: thanks bob, good seeing you

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