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0:05
OUR FIRST SPEAKER TODAY IS NEIL CAPORASO, HE GOT HIS M.D. FROM THE UNIVERSITY OF MEDICINE AND DENTISTRY OF NEW JERSEY IN 198O RESIDENCY IN INTERNAL MEDICINE AND JOINED NCI AS ONCOLOGY FELLOW IN THE MEDICINE BRANCH. HE BECAME A BIOTECHNOLOGY FELLOW IN THE ENVIRONMENTAL EPIDEMIOLOGY BRANCH AT NCI, AND THEN BECAME CHIEF OF THE GENETIC EPIDEMIOLOGY BRANCH IN 2011, HE'S NOW IN THE OCCUPATIONAL AND ENVIRONMENTAL STUDIES BRANCH AND HE'S GOING TO TALK TO US ABOUT EPIDEMIOLOGY. NEIL. >> THANK YOU.
0:56
WELCOME EVERYBODY. AND I'M GOING TO GIVE YOU A RAPID INTRODUCTION TO EPIDEMIOLOGY. WHICH IS A POPULATION PERSPECTIVE ON CANCER. SO MANY OF YOU ARE CLINICIANS, BUT EPIDEMIOLOGISTS WORRY ABOUT THE POPULATION AS A WHOLE. I'M GOING TO COVER WHAT IS EPIDEMIOLOGY, WHAT ARE THE ACCOMPLISHMENTS, WHAT CAN GO WRONG OR WHAT ARE THE CHALLENGES, A CASE STUDY OF WHAT CAN GO REALLY WRONG, AND THEN I'LL TAKE A PEEK AT THE FUTURE. SO WHAT IS EPIDEMIOLOGY? AND I LOOKED FOR ONE SLIDE THAT
1:39
COULD KIND OF CONVEY WHAT EPIDEMIOLOGY TRIES TO DO. I THINK THIS SLIDE CAPTURES IT. IF YOU ALLOW MARKET FORCES TO TELL US WHAT'S GOOD FOR US AND WHAT'S BAD FOR US, YOU JUST HAVE TO GO BACK A FEW DECADES AND YOU CAN SEE THAT ADVERTISERS USED IMAGES OF DOCTORS TO SELL US CIGARETTES. PROBABLY THE BEST ESTABLISHED ASSOCIATION IN ALL OF EPIDEMIOLOGY IS THAT SMOKING CAUSES LUNG CANCER. SO WE REALLY NEED A SCIENTIFIC DISCIPLINE THAT STEPS IN AND EXAMINES THE CAUSES OF CANCER.
2:18
IF YOU SAY TO YOURSELF, WELL, THAT WAS THEN, WHAT ABOUT NOW, THERE ARE POTENTIAL CAUSES OF CANCER AND HUMAN DISEASE THAT MAYBE TODAY WE DON'T REALLY SUSPECT. AND I THINK HALLOWEEN IS A GOOD TIME TO RAISE THE ISSUE OF SUGAR. SO I WILL COME BACK TO THIS A LITTLE BIT LATER IN THE TALK. OKAY. SO WHAT IS EPIDEMIOLOGY? IT'S CONCERNED WITH THE HUMAN POPULATION, AND IT'S AN OBSERVATIONAL SCIENCE, LIKE ASTRONOMY, FOR EXAMPLE, AND CONTRAST THAT WITH EXPERIMENTAL SCIENCE. IN EPIDEMIOLOGY, WE'RE NOT
2:59
ALLOWED TO ADMINISTER POTENTIALLY HARMFUL TREATMENTS TO PEOPLE. WE CAN'T ASSIGN 50 PEOPLE TO THE SMOKING GROUP AND 50 TO THE NON-SMOKING GROUP, BUT WE HAVE TO OBSERVE THEIR CURRENT STATUS. SO THAT'S WHY IT'S CALLED AN OBSERVATIONAL SCIENCE. THE WORK OF EPIDEMIOLOGY TAKES PLACE IN NCI IN A DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS. AND I'M CURRENTLY WORKING IN THE OCCUPATION ENVIRONMENTAL EPIDEMIOLOGY BRANCH WHERE WE'RE FOCUSED ON ENVIRONMENTAL AND OCCUPATIONAL CAUSES OF CANCER.
3:40
SO, EPIDEMIOLOGY IN DCEG HAS CONTRIBUTED TO REGULATORY CHANGES, CLINICAL PRACTICE, AND PREVENTIVE INTERVENTIONS. I'LL GIVE A FEW SPECIFIC EXAMPLES AS WE GO FORWARD. JUST TO ORIENT YOU TO WHERE WE ARE, NCI IS PART OF NIH, AND OUR DIVISION, DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS, IS INTRAMURAL. 85% OF THE DOLLARS GO EXTRAMURALLY TO GRANTS, BUT THE INTRAMURAL PART IS A VERY IMPORTANT COMPONENT. AND IN THE DIVISION OF CANCER EPIDEMIOLOGY AND GENETICS THERE ARE A NUMBER OF BRANCHES IN
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ADDITION TO OURS WHICH IS OF COURSE THE MOST IMPORTANT. THERE ARE BRANCHES CONCERNED WITH METABOLIC FACTORS LIKE NUTRITION AND HORMONES, INFECTION GENETICS STATISTCS RADIATION. OUR WORK FOCUSES ON DEVELOP AND GENETIC CAUSES OF CANCER IN THE POPULATION, HIGH QUALITY/HIGH IMPACT EVALUATED RESEARCH. THERE ARE STUDIES NATIONAL AND INTERNATIONAL IN SCOPE, AND WE HAVE A LOT OF SCIENTIFIC PARTNERSHIPS WITH LABORATORIES INVESTIGATING MOLECULAR EPIDEMIOLOGY OF CANCER. THE NEXT SPEAKER ALREADY
5:10
FOCUSING ON HEALTH DISPARITIES KEY IN INTERNATIONAL STUDIES. SO, JUST TO MENTION, OUR STUDIES ARE WORLDWIDE. SO WE HAVE INVESTIGATIONS IN CHINA, AND THIS HAS BEEN FOR DECADES, PRETTY OF ALL OVER THE WORLD, INCLUDING PLACES YOU MIGHT NOT SUSPECT LIKE IRAN THROUGH SOUTH AMERICA, AFRICA, AND OF COURSE ALL ACROSS THE UNITED STATES. SO THERE'S A NICE WEBSITE THAT YOU CAN VISIT, AND YOU CAN LEARN ABOUT OUR SPECIFIC STUDIES AND THE INVESTIGATORS AND THERE'S A LOT OF GREAT INFORMATION THERE. ALSO TOOLS.
5:50
SO BREAST, MELANOMA, COLORECTAL, ASSESSMENT TOOLS. SO BACK TO OBSERVATIONAL VERSUS EXPERIMENTAL, AS I MENTIONED, EPIDEMIOLOGISTS ARE ETHICALLY PROHIBITED FROM PERFORMING EXPERIMENTS ON PEOPLE SO WE OBSERVE LARGE POPULATIONS AND THEN RELATE THEIR OUTCOMES TO WHAT PEOPLE DO TO KEY EXPOSURES. THE WEAKNESS OF OBSERVATIONAL STUDIES WAS SOMETHING THAT WAS EXPLOITED BY THE TOBACCO COMPANIES WHEN THE FIRST STUDIES EMERGED RELATING TOBACCO TO CANCER. THEY SAID, WELL, THIS DOES
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REALLY NOT HAVE A FIRM BASIS, AND HOW DO YOU KNOW IT'S NOT SMOKING BUT IT'S THE PERSONALITY, SMOKERS HAVE A MORE ADVENTUROUS OUTGOING PERSONALITY AND THAT MAY BE WHAT REALLY CAUSES THE LUNG CANCER, ASSOCIATION. SO EPIDEMIOLOGISTS FROM THE BEGINNING HAVE BEEN CONCERNED WITH ESTABLISHING CAUSALITY. I'LL GIVE SOME EXAMPLES OF THAT IN A SECOND. STUDIES IN TERMS OF THE STRENGTH OF ESTABLISHING EVIDENCE OF CAUSALITY. AND THE WEAKEST STUDIES ARE ANECDOTES. IN OTHER WORDS, I HEARD SOMEBODY
7:13
ATE WHEAT GERM AND LIVED TO BE 90. OKAY, THAT'S NICE, BUT THE SECOND LEVEL WOULD BE SMALL UNREPRESENTATIVE SAMPLES, SAMPLES OF CONVENIENCE, SO TO SPEAK. THEN CROSS-SECTIONAL, ALSO KNOWN AS PREVALENCE STUDIES, THE PROBLEM IS THEY ARE BIASED BY DIFFERENTIAL SURVIVAL. THERE'S A RANGE OF QUALITY IN ALL THESE KINDS OF STUDIES. GENERALLY THE NEXT LEVEL, COHORT STUDIES HAVE THE ADVANTAGE OF IDENTIFYING A LARGE GROUP PROSPECTIVELY AND FOLLOWING THEM OVER TIME FOR DIFFERENT OUTCOMES.
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AND SO THEY TEND TO AVOID SELECTION BIAS TO SOME DEGREE THAT PLAGUES CASE CONTROL STUDIES. AND FINALLY RANDOMIZED CLINICAL TRIALS ARE THOUGHT TO BE THE HIGHEST LEVEL OF EVIDENCE. GOALS OF EPIDEMIOLOGY IDENTIFY CAUSES OF CANCER, QUANTIFY RISKS, EPIDEMIOLOGISTS ARE VERY CONCERNED WITH PUBLIC HEALTH, AND PUBLIC HEALTH SERVICES, HOW MUCH IS NEEDED, HOW MANY CASES OF BREAST CANCER ARE WE GOING TO HAVE NEXT YEAR AND WHAT KINDS OF HEALTH SERVICES DO WE NEED TO SUPPORT THEM.
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WE WANT TO IDENTIFY SYNDROMES, TRENDS AND EPIDEMIC, AND WE WANT TO UNDERSTAND MECHANISMS. EPIDEMIOLOGISTS TEND TO 'EM -- EMPHASIZE P ROTECTIONS, CHEAPER THAN TREATMENT, A GOOD APPROACH. WE WANT TO ELIMINATE DISEASE AT THE SOURCE, GENERALLY REQUIRES EDUCATION COMMUNICATION. THERE'S A BIG DOWN SIDE TO PREVENTION. AND THAT'S A POLITICAL ISSUE. THE ISSUE IS THIS. YOU CAN'T GO TO CONGRESS AND POINT TO ALL THE CASES OF A CONDITION THAT YOU PREVENTED. YOU CAN SHOW THE EVIDENCE, BUT
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IT'S NOT LIKE YOU HAVE GRATEFUL PATIENTS THAT ARE SAYING YES BECAUSE YOU GAVE ME THE LATEST TREATMENT, I'M NOW ALIVE, YOU HAVE A LOT OF PEOPLE WITHOUT DISEASE. SO YOU HAVE TO RELY ON STATISTICS, THEY ARE INHERENTLY LESS GERMANIC THAN TREATMENT. IT'S HARDER TO GET FUNDING FOR PUBLIC HEALTH EVEN THOSE MORE EFFECTIVE. IT TAKES TIME. IF WE ELIMINATE AN EXPOSURE NOW, IT MAY TAKE DECADES FOR THIS TO SHOW UP IN HEALTH STATISTICS. AND FINALLY, EPIDEMIOLOGISTS DON'T TEND TO GET NOBEL PRIZES.
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SO THIS IS A DOWN SIDE FOR THE INDIVIDUALS, AND IT'S NOT A BIG DEAL BUT REALLY FOR THE SCIENTISTS THAT IDENTIFIED TOBACCO AS A CARCINOGEN AND DID THOSE FIRST STUDIES, I THINK THAT YOU COULD ARGUE THEY SAVED MORE LIVES THAN VIRTUALLY ANY OTHER INTERVENTION YOU CAN IMAGINE, AND THEY CERTAINLY ARE DESERVING. OKAY. EPIDEMIOLOGISTS ARE CONCERNED WITH BIAS, SYSTEMATIC DEVIATION FROM THE TRUTH, AND THIS COULD BE AN ENTIRE ONE-HOUR TALK EASILY BUT I'M GOING TO GIVE YOU ONE EXAMPLE.
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AND THAT IS THAT YOU COULD HAVE A BIAS, IT'S EXTREMELY COMMON, IN VIRTUALLY ANY STUDY BASED ON THE PARTICIPATION RATE.& AND THIS IS BECAUSE IF YOU ONLY HAVE A SMALL PROPORTION OF PEOPLE WHO ARE ELIGIBLE FOR A STUDY PARTICIPATING, YOU DON'T KNOW IF THEY ARE REALLY REPRESENTATIVE OF THE TARGET POPULATION AND THEY MAY NOT BE GENERALIZABLE TO THE GENERAL POPULATION. SO THAT'S A CONCERN. AND IF I WAS TO ASK YOU AN EXAMPLE OF A GIGANTIC STUDY, LIKE U.K. BIOBANK IN ENGLAND, WHAT PERCENTAGE OF ELIGIBLE
11:54
PEOPLE ACTUALLY PARTICIPATE IN THAT STUDY? THE PERCENTAGE TURNS OUT TO BE EXTREMELY SMALL, ABOUT 5% OR LESS. SO THAT POPULATION IS PROBABLY BIASED AND ALTHOUGH IT IS SOMEWHAT GENERALIZABLE AND WE USE THAT STUDY ALL THE TIME, VERY, VERY DIFFICULT TO GET A HIGHLY GENERALIZABLE POPULATION. SO AS ONE EXAMPLE, MY GROUP DID A LARGE CASE CONTROL STUDY AT THE TIME, WE DID THIS, IT WAS THE LARGEST CASE CONTROL STUDY IN THE WORLD OF LUNG CANCER, 2,000 CASES AND 2,000 CONTROLS. AND WHEN WE INITIALLY DID A
12:33
PHONE SURVEY, THIS WAS IN MILAN, ITALY, TO DETERMINE WHETHER PEOPLE WOULD AGREE TO THE STUDY ONLY 30% OF THE POPULATION OF FOLKS WE CALLED SAID, YEAH, WE'D PARTICIPATE IN THAT STUDY. AND OUR SITE VISIT AT THAT TIME SAID NO, NO, NO, YOU CAN'T DO THAT. WE CAN'T HAVE THAT. YOU EITHER HAVE TO INCREASE THE PARTICIPATION RATE OR WE'RE NOT GOING TO GIVE YOU THE $12 MILLION YOU NEED FOR THE STUDY. SO WE SPENT A YEAR, AND WE DID INVITATION LETTERS, FOLLOW-UP BY PHONE ADVERTISEMENTS OFFERED
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THEM CASH, GOT A LETTER FROM THEIR PHYSICIAN AND OFFERED TO STUDY THEM AT THE HOSPITAL OR AT HOME. THAT INCREASED PARTICIPATION TO 49%. FINALLY THE TWO KEY THINGS WE GOT EXTREMELY CHARMING INTERVIEWERS OF THE OPPOSITE SEX, AND WE GAVE THEM GAS COUPONS WHICH AT THE TIME IN ITALY WAS EXTREMELY DESIRABLE. AND WE HAD SOME OTHER -- WE HAD A LETTER FROM THE MAYOR. THEY ACTUALLY LIKED THE MAYOR, THAT WAS A GOOD THING. WE GOT THE PARTICIPATION RATE IN CONTROLS UP TO 70%. IT WAS EASIER TO GET CASES
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BECAUSE THEY WERE IN THE HOSPITAL. SO THAT'S AN EXAMPLE OF WHAT YOU HAVE TO DO TO IMPROVE YOUR PARTICIPATION RATE, AND THAT EFFORT TOOK A YEAR AND COST A MILLION DOLLARS. OKAY. EPIDEMIOLOGISTS WORRY ABOUT CONTROLS, AS I SAID IT CAN BE EXPENSIVE TO GET REALLY GOOD CONTROLS. YOU WANT THEM TO BE REPRESENTATIVE. HAVING POPULATION CONTROLS LETS YOU DO SOME THINGS COMPUTATIONALLY THAT NORMALLY YOU COULDN'T DO. AN EXAMPLE IS YOU COULD CALCULATE ABSOLUTE RATES AS OPPOSED TO RELATIVE RISKS.
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NOW, RELATIVE RISKS ARE VERY USEFUL. FOR EXAMPLE, I COULD TELL YOU THAT USING HAIR SPRAY INCREASES THE RELATIVE RISK OF LYMPHOMA BY 1.4 TO 1.6. THAT'S A 40 TO 60% INCREASED RATE, BUT IS THAT RELEVANT TO AN INDIVIDUAL PATIENT? NO. YOUR ABSOLUTE RISK IS STILL TINY. IT'S VERY IMPORTANT TO UNDERSTAND DIFFERENCE BETWEEN ABSOLUTE AND RELATIVE RISK. AND I MENTIONED TO YOU ALREADY THAT CONVENIENCE CONTROLS ARE THE LEAST DESIRABLE. SO, IF YOU SEEK AN EPIDEMIOLOGIST AS A CONSULTANT
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BECAUSE YOU WANTS TO DO A STUDY, THE KINDS OF QUESTIONS THEY ARE GOING TO ASK YOU, WHAT'S YOUR STUDY DESIGN, WHERE DID YOU GET YOUR CONTROLS, DID YOU COLLECT KEY COVARIATES TO TAKE INTO ACCOUNT CONFOUNDING? AND DETERMINE IF YOUR CASE AND CONTROL POPULATIONS ARE SIMILAR? DID YOU CONSIDER BIAS? WHAT WAS YOUR ORIGINAL HYPOTHESIS? AND NOW THAT YOU HAVE YOUR DATA, ARE YOU LOOKING AT OTHER HYPOTHESES? IF SO YOU REALLY SHOULD BE CONSIDERING MULTIPLE COMPARISONS IN YOUR STATISTICAL APPROACH.
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HAVE YOU DONE POWER CALCULATIONS SO YOU KNOW WHAT KIND OF EFFECT YOUR STUDY SIZE PERMITS YOU TO DETECT? AND WHAT KIND OF VALIDATION DID YOU DO IF YOU DID BIOMARKERS? THE MOST COMMON QUESTION EPIDEMIOLOGISTS GET IS CAN YOU EXPLAIN TO ME WHY MY GRANDMOTHER, WHO SMOKED ALL HER LIFE, ATE BACON, OUTLIVED HER DOCTORS, HOW CAN YOU EXPLAIN THAT? SHE HAD ALL THESE UNHEALTHY LIFESTYLE FACTORS. AND ONE ANSWER TO THIS, THERE'S A LOT OF DIFFERENT ANSWERS, IS THAT EPIDEMIOLOGY IS CONCERNED
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WITH PROBABILISTIC FACTORS, NOT DETERMINISTIC, AND WE KNOW A LOT OF THINGS ASSOCIATED WITH CANCER BUT DON'T KNOW IF A GIVEN INDIVIDUAL WILL HAVE A SPECIFIC OUTCOME OF INTEREST. SO, RISK IS NORMALLY DISTRIBUTED, AND YOU'RE ALWAYS GOING TO GET PEOPLE AT THE END OF THAT DISTRIBUTION. OKAY. I'M GOING TO TOUCH ON A FEW TOOLS THAT EPIDEMIOLOGISTS USE THAT ARE USEFUL. ONE IS CANCER MAPS. AND HERE, FOR EXAMPLE, IS A MAP OF MELANOMA DISTRIBUTION, AND WHAT DOES THIS MAP TELL YOU THAT
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WOULD BE REALLY HARD TO FIGURE OUT IN ANY OTHER WAY? AS SOON AS WE LOOKED AT THIS MAP WHAT'S OBVIOUS IS THAT IT HAS SOMETHING TO DO WITH SUN BECAUSE AS YOU GO SOUTH RATES OF MELANOMA INCREASE. TODAY MORE SOPHISTICATED APPROACHES GEOGRAPHIC INFORMATION SYSTEMS, BASED ON SATELLITE DATA, IS USED TO STUDY A WIDE VARIETY OF EXPOSURES, AND THIS IS INCREASINGLY COMMON AND USED FOR ALL SORTS OF STUDIES IN EPIDEMIOLOGY. SEAR SURVEILLANCE EPIDEMIOLOGY AND END RESULTS, COVERS A
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QUARTER OF THE U.S. POPULATION, 11 DIFFERENT STATES, GENERATES EXTREMELY DETAILED HEALTH STATISTICS ON CANCER. AND SO THIS IS A TOOL THAT ANYONE CAN USE. YOU CAN GO ONTO THE SEER WEBSITE AND DOWNLOAD CANCER FACTSHEETS, IT'S EASY TO DO YOUR STATISTICS AND ASK DIFFERENT QUESTIONS IF YOU WANT. WHAT DO YOU LEARN FROM SEER DATA? I'LL SHOW YOU A SOURCE OF BIAS. HERE ARE RATES OF CANCER ACROSS DIFFERENT RACES, FROM 1975 TO 2000. OH, LOOK IN MEN THERE'S A BIG JUMP IN THE CANCER RATES IN THE EARLY '90s.
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WE DON'T SEE IT IN WOMEN. WHAT HAPPENED THERE? HERE'S THE ANSWER. YOU CAN SEE THE RATES OF A VARIETY OF CANCERS ARE RELATIVELY FLAT, BUT PROSTATE JUMPED UP. AND WHAT HAPPENED RIGHT AROUND THIS TIME? PSA SCREENING WAS INTRODUCED. AND SO WHAT HAPPENED WAS YOU HAD EARLY DETECTION OF A VARIETY OF CANCERS DURING THIS PERIOD. AND HERE'S THE DISTRIBUTION BY RACE, AND IT'S WELL KNOWN THAT AFRICAN-AMERICAN MEN HAVE HIGHER RATES THAN WHITE MEN. AND YOU SEE DISTRIBUTION THERE. HERE'S ANOTHER THING YOU CAN
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LOOK AT IN SEER, THE DIFFERENCE BETWEEN INCIDENCE AND MORTALITY. WHAT DOES IT MEAN IF A SPECIFIC CANCER HAS A BIG DIFFERENCE BETWEEN INCIDENCE AND MORTALITY? WELL, ONE THING IT MEANS IS THAT THAT PARTICULAR CANCER MAY BE AMENABLE TO SUCCESSFUL TREATMENT. SO IT REFERS TO CHILDHOOD CANCER, WHERE A LOT OF CANCERS HAVE A GREAT SUCCESS RATE. FOR EXAMPLE, CHILDHOOD A.L.L. BETTER THAN 90% CURE RATE. I SAID I WOULD TOUCH ON CAUSATION, EPIDEMIOLOGISTS HAVE BEEN CONCERNED WITH DO YOU PROVE
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A CAUSE, AND BRADFORD HILL, WAY BACK IN THE '60s, IDENTIFIED SOME CRITERIA THAT ARE ASSOCIATED WITH TRUE CAUSAL FACTORS. ONE IS YOU WANT A HIGH RELATIVE RISK OR ODDS RATIO. SO IF YOU HAVE A RISK OF 1.2, THAT MAY WELL BE BIAS THAT'S CAUSING THAT. IF YOU HAVE A RISK OF 12, THAT TENDS TO BE SOMETHING THAT YOU WANT TO THINK ABOUT AS TRUE CAUSE. YOU'D LIKE WHATEVER YOU IDENTIFY AS CAUSAL TO BE CONSISTENT. YOU'D LIKE TO SEE A DOSE-RESPONSE IF YOU HAVE MORE OF THE CAUSE, YOU'D LIKE TO HAVE
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MORE OF THE CANCER. THE CAUSE SHOULD PRECEDE THE OUTCOME TEMPORALLY OR IT'S NOT A GOOD IDEA THAT IT'S A CAUSE. FINALLY YOU WOULD LIKE BIOLOGIC PLAUSIBILITY. TODAY AT LEAST I'LL MENTION THERE ARE NEWER APPROACHES TO IDENTIFYING CAUSALITY. ONE OF THEM IS MEDIATION ANALYSIS, AND THIS REFERS TO WHEN YOU HAVE AN INDEPENDENT VARIABLE AND DEPENDENT VARIABLE AND HAVE YOU AN INTERMEDIARY VARIABLE IN BETWEEN THEM. AND SO MEDIATION ANALYSIS INVOLVES MATHEMATICAL TECHNIQUES TO RELATE EACH TO THE OTHER AND
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TRY TO INFER SOMETHING ABOUT CAUSE. MENDELIAN RANDOMIZATION REFERS TO USING GENETIC MARKERS TO INFER CAUSALITY. SO THE WAY THIS WORKS IS SUPPOSE WE WANT TO UNDERSTAND IF TOBACCO REALLY IS A CAUSAL FACTOR IN LUNG CANCER. WELL, YOU CAN -- IF YOU HAVE GENES THAT PREDISPOSE PEOPLE TO SMOKING, WHICH THROUGH GWAS STUDIES IN FACT WE DO HAVE, WHAT YOU CAN DO IS IDENTIFY A GROUP OF THOSE GENES AND GIVE PEOPLE WITH LUNG CANCER A SCORE BASED ON THOSE GENES, AND DETERMINE IF IN FACT THEY HAVE MORE OF THOSE
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GENES THAN YOU'D EXPECT. AND IN FACT WHEN THAT KIND OF ANALYSIS IS DONE, YOU DO FIND EVIDENCE FOR CAUSALITY WITH TOBACCO AND LUNG CANCER, BUT FOR OTHER INTERESTING ASSOCIATIONS YOU DON'T FIND IT. A CLASSICAL EXAMPLE OF THAT IS HDL CHOLESTEROL AND HEART DISEASE. SO DRUG COMPANIES HAVE TRIED TO DEVELOP DRUGS THAT ACTUALLY RAISE HDL CHOLESTEROL, IT'S THOUGHT TO BE PROTECTIVE, BUT WHEN YOU DO A MENDELIAN RANDOMIZATION ANALYSIS YOU FIND NO EVIDENCE FOR CAUSALITY, SO THERE'S LIKELY SOME OTHER FACTOR
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ASSOCIATED WITH BOTH HDL CHOLESTEROL THAT HAS THE REAL EFFECT THAT MIGHT BE EXERCISE OR MIGHT BE INSULIN RESISTANCE. OH, MOLECULAR EPIDEMIOLOGY, THIS REFERS TO USING BIOMARKERS IN EPIDEMIOLOGY STUDIES TO HELP DEFINE MECHANISMS. I'LL COME BACK TO MOLECULAR EPIDEMIOLOGY IN A MINUTE. HERE'S AN EXAMPLE OF ONE OF THE EARLY COHORT STUDIES THAT SHOWED A BEAUTIFUL DOSE-RESPONSE BETWEEN CIGARETTES SMOKED PER& DAY AND RATES OF LUNG CANCER. I'M LOOKING AT THE CLOCK BECAUSE I WILL END WITH AT LEAST TEN
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MINUTES BEFORE THE END TO ALLOW FOLKS A CHANCE TO ASK QUESTIONS. HERE'S TEMPORAL ISSUES, SO YOU CAN SEE MALE SMOKING INCREASED IN THE POPULATION REALLY DECADES BEFORE THE RATES OF LUNG CANCER INCREASED. SAME THING WITH WOMEN. AND HERE ARE ANIMAL STUDIES THAT SHOWED PRE-MALE PLASTIC CHANGES IN BRONCHIAL EPITHELIUM THAT WERE SIMILAR TO THOSE SEEN IN HUMANS, IN DOGS THAT WERE PUT ON SMOKING MACHINES. THIS EARLY STUDY INCREASED BIOLOGICAL PLAUSIBILITY THAT TOBACCO WAS THE CAUSAL FACTOR.
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YOU COULDN'T EXPLAIN THIS BY SAYING THE BEAGLES HAD DIFFERENT PERSONALITIES. AND HERE'S ANOTHER GREAT EPIDEMIOLOGIC STUDY. THESE ARE COHORTS WHERE YOU HAD PEOPLE THAT QUIT SMOKING AND YOU COULD SEE THAT AS THEY QUIT SMOKING, OVER TIME THE RATES OF LUNG CANCER IN A VERY CONSISTENT WAY ACROSS THREE DIFFERENT COHORTS DECLINED. OKAY. SO LET ME TOUCH ON SOME OF EPIDEMIOLOGY'S ACCOMPLISHMENTS. SO IN GENERAL, EPIDEMIOLOGISTS HAVE BEEN SUCCESSFUL IN IDENTIFYING SOME OF THE GENERAL
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AND SPECIFIC CAUSES OF CANCER. THEY HAVE BEEN ADVOCATES OF PUBLIC HEALTH. I WILL TOUCH ON TOBACCO AGAIN. THE ROLE OF SECONDARY TOBACCO SMOKE I THINK IS REALLY IMPORTANT AND I'M GOING TO SAY A WORD ABOUT MOLECULAR EPIDEMIOLOGY. IN DCEG IN ADDITION TO VARIOUS STUDIES IN PARTICULAR AREAS, OFTEN CONGRESS OR A PAPER WILL COME OUT AND NCI WILL CALL ON EXPERTS IN DCEG TO MAKE A COMMENT AND TO DISCUSS DIFFERENT CANCER CAUSES. SO THAT'S HAPPENED WITH SILICONE BREAST IMPLANTS, CHERNOBYL, ORAL
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CANCER AND MOUTHWASH, ABORTION AS A POSSIBLE CAUSAL FACTOR IN BREAST CANCER WHICH IT IS NOT, CELL PHONES, AND FOR FUKUSHIMA FOLKS IN RADIATION EPIDEMIOLOGY BRANCH ACTUALLY WENT OVER THERE TO HELP CONSTRUCT STUDIES TO FOLLOW THE POPULATION IN TERMS OF CANCER RISK. WHAT ARE THE GENERAL RISK FACTORS FOR CANCER? IT'S AGE, ENVIRONMENTAL FACTORS, GENETICS AND COMBINATION. SPECIFIC CAUSES, TOBACCO IS RESPONSIBLE FOR A THIRD OF CANCER. DIET CERTAINLY CONTRIBUTES, IT'S HIGHLY PROBLEMATIC WHAT THE
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DIETARY CAUSES, AND ALL OTHERS CONTRIBUTE TO A THIRD. IT'S A RULE OF THUMB MOST CANCER IS DUE TO THE ENVIRONMENT. AND THAT'S BECAUSE VARIATION BY GEOGRAPHY AND OVER TIME ONLY ARE COMPATIBLE WITH EXTRINSIC ENVIRONMENTAL QUESTIONS. THERE'S A VAST BODY OF DESCRIPTIVE ECOLOGICAL AND ANALYTICAL DATA THAT ESTABLISHES THIS. BY THE WAY WHEN I SAY THE WORD ANALYTIC EPIDEMIOLOGY IT REFERS TO DEFINED CASE CONTROL AND COHORT STUDIES, WHERE CONFOUNDERS ARE TAKEN INTO ACCOUNT. SO HERE'S A STUDY THAT COULD BE
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IN THE NEXT TALK ON HEALTH DISPARITIES, BUT WHAT THIS POINTS OUT IS THAT THE HIGHEST -- THE RATIO OF HIGHEST TO LOWEST RELATIVE RISKS ACROSS COUNTRIES IS DRAMATIC. SO CANCER RISK FACTORS REALLY DO VARY GREATLY, AND SO THIS TENDS TO POINT TO ENVIRONMENTAL FACTORS. NOW, YOU MIGHT RAISE THE QUESTION, WELL, HOW DO YOU KNOW IT'S NOT GENETIC? I MEAN ASIANS HAVE A DIFFERENT GENE POOL TO SOME DEGREE THAN AFRICAN-AMERICANS AFRICANS OR CAUCASIANS. IN FACT WE KNOW THAT FROM MIGRATION STUDIES.
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SO WHEN FOLKS MIGRATE FROM ONE STUDY TO THE OTHER, ONE COUNTRY TO ANOTHER, WITH THE EXCEPTION OF A FEW CANCERS THAT I'LL MENTION, THEY TEND TO RAPIDLY ASSUME THE CANCER RATES OF THE NEW COUNTRY. OUR CANCER MAPS HELP US IMPLICATE EXPOSURE. A NICE EXAMPLE IS FROM ONE OF THE FIRST CANCER MAPS OF LUNG CANCER WHICH FOUND THIS HIGH RISK AREA IN MONTANA, AND WHAT WAS IN THIS AREA BUT A COPPER SMELTING PLANT CONTAMINATED WITH ARSENIC. THIS PLANT WAS REMOVED, AND WHEN IT WAS REMOVED THE CANCER RATES
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IMPROVED. AND THAT RED AREA WENT AWAY. ANOTHER EXAMPLE IS XUAN WEI IN CHINA WHERE WE'VE HAD STUDIES FOR A FEW DECADES, THE HIGHEST RISK OF LUNG CANCER IN CHINA. WHAT DO YOU FIND? YOU FIND INDOOR AIR POLLUTION. YOU FIND BEDS THAT BURN SMOKY COAL, AND ARE POORLY VENTED IN HOUSES. SO FOLKS BREATHE IN THIS SMOKE AND IT'S AS GOOD AS SMOKING A LOT OF CIGARETTES. AND IT RESULTS IN HIGHER CANCER RATES. AND STUDIES WHEN THEY REMOVE THESE INDOOR SOURCES OF AIR POLLUTION SHOW THAT THE RATES OF
29:30
CANCER DRAMATICALLY DECLINE. OKAY. SO CIGARETTES ARE THE BIG HITTER. AND I WILL SAY A WORD ABOUT TOBACCO THAT, YOU KNOW, THIS IS SOMETHING YOU CAN LOOK AT LATER BUT IT IS STILL THE MAJOR CAUSE OF PREVENTIBLE MORBIDITY AND MORTALITY, AND IT'S HARD TO BELIEVE BUT IN THIS CENTURY IT'S STILL EXPECTED TO CAUSE HUNDREDS OF MILLIONS OF DEATHS. SO THAT'S BECAUSE IN THE DEVELOPING WORLD, CIGARETTES ARE STILL HEAVILY MARKETED, IN SPITE OF THE DECLINE IN THE UNITED STATES AND EUROPE, IN CHINA AND
30:09
INDIA AND OTHER AREAS SMOKING IS STILL GOING STRONG. SMOKING STRONGLY ASSOCIATED WITH SEVEN CANCERS AND WE STILL DO STUDIES, NICE STUDY BY NEIL FREEMAN SHOWING ASSOCIATION BETWEEN SMOKING AND BLADDER CANCER RISK. IT TAKES DECADES TO CHANGE BEHAVIOR. THIS IS THE SURGEON GENERAL'S REPORT IN THE LATE '60s. FIRST STUDIES OF TOBACCO IN CANCER IN THE '50s, AND THE RATE OF SMOKING IN THE UNITED STATES IN ADULTS HAS SLOWLY DECLINED. SO IT'S ABOUT 12, 13% AMONG ADULTS TODAY BUT CERTAIN AREAS
30:51
OF THE COUNTRY IT'S MUCH HIGHER. ONE OF THE EFFECTS OF DECLINE IN THE RATE OF SMOKING THAT MAYBE YOU'RE NOT AWARE OF, IT WAS SHOWN A DECADE LATER THAT ENVIRONMENTAL TOBACCO SMOKE WAS A RISK FACTOR FOR THE SPOUSES OF SMOKERS. AND THIS IN TURN LED TO CLEAN AIR LAWS. THAT ELIMINATED SMOKING ON AIRPLANES, PUBLIC BUILDINGS, MOVIES, HOSPITALS, ALL THOSE PLACES WHERE YOU WOULD GO IN AND HAVE TO BREATHE OTHER PEOPLES SMOKE. SO THIS WAS A TERRIFIC PUBLIC HEALTH BOON, AND INCALCULABLE
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NUMBERS OF LIVES HAVE BEEN SAVED AND BASED ON THIS CLEAN AIR LEGISLATION. SO THIS IS REALLY SOMETHING YOU CAN THANK EPIDEMIOLOGISTS FOR. I JUST WANTED TO MENTION THERE'S A LOT OF RESEARCH TODAY ON SMOKING. AND THIS IS A PAPER WE DID JUST IN THE LAST YEAR, WHERE WE LOOKED AT THE RATES OF LIGHT AND INTERMITTENT SMOKING. AND THIS IS THE FASTEST-GROWING SEGMENT IN SMOKERS OVER THE LAST 15 YEARS. AND THIS REFERS TO SMOKERS THAT SMOKE NOT EVERY DAY. AND LESS THAN FIVE CIGARETTES PER DAY.
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SO THESE SMOKERS DO IS THAT THEY MAY GET TOGETHER WITH THEIR FRIENDS OR GO TO A BAR AND HAVE A CIGARETTE, OR MAY SNEAK OUT OF THE HOUSE BECAUSE THEIR SPOUSE DOESN'T WANT THEM TO SMOKE. FOR WHATEVER REASON, THEY SMOKE INTERMITTENTLY. THESE SMOKERS FROM UNIQUE CHARACTERISTICS. SO THERE ARE DIFFERENCES BY ETHNIC GROUP, BY EDUCATION, BY AGE. PROBABLY THE BIGGEST DIFFERENCE IS THAT THEY ARE LESS DEPENDENT SMOKERS. THEY HAVE LESS NICOTINE DEPENDENCY. SO WE FOLLOWED THIS WITH A STUDY
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AGAIN LED BY OTHER INVESTIGATORS THAT SHOWED THAT EVEN IF YOU SMOKE A LITTLE BIT, YOUR ALL-CAUSE MORTALITY WAS SHARPLY INCREASED. SO EVEN SMOKING THAT SMALL AMOUNT, AND YOU'D EXPECT THIS BASED ON THE DATA, ON SPOUSAL SMOKING, OR SMOKING IN THE WORKPLACE, OR SMOKE INCOME THE FAMILY, THAT THE RATE OF LUNG CANCER WAS INCREASED, AND SO IS THE RATE OF MORTALITY. SO SMOKING IS STILL AN ONGOING CONCERN, EVEN TODAY. OKAY. I'M NOT GOING TO SPEND TOO OF TIME ON THE OTHER MAJOR RISK FACTORS OF CANCER.
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THIS IS SOMETHING YOU CAN LOOK UP ON YOUR OWN. BUT ALCOHOL IS NUMBER TWO AFTER SMOKING, ASSOCIATED WITH A VARIETY OF CANCERS. SOMETIMES EPIDEMIOLOGISTS DO SOME GOOD BY PROVING THAT A PARTICULAR FACTOR IS NOT ASSOCIATED WITH CANCER. SO IT TURNS OUT THAT COFFEE DRINKING IS ACTUALLY GOOD FOR YOU IN MANY WAYS. GOOD FOR YOUR LIVER, GOOD FOR CARDIOVASCULAR ENDPOINTS, AND SLIGHTLY LESS ALL-CAUSE MORTALITY. IONIZING RADIATION IS RESPONSIBLE FOR A VARIETY OF CANCERS. I'M NOT GOING TO GO INTO THAT.
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A LOT OF STUDIES FROM OUR GROUP. I'M NOT GOING INTO NON-IONIZING RADIATION, TANNING BEDS. A LOT OF RESEARCH HAS GONE INTO INFECTIONS IN CANCER. IT'S A MAJOR ETIOLOGIC FACTOR IN CANCERS INCLUDING NEWER INFECTIOUS HYPOTHESES. AND I'M NOT GOING TO GO INTO MICROBIOME AND HOW THAT HAS NOW IMPLICATED SOME CAUSES OF CANCER, PROBABLY THE BEST STUDIED IS FUSO BACTERIUM, A LOT OF STUDIES ARE TRYING TO NAIL DOWN THE ASSOCIATION OF THIS BUG WITH COLORECTAL CANCER. AND IN CERVICAL CANCER THE
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DIFFERING ASSOCIATION OF DIFFERENT STRAINS OF HPV WITH CANCER WITH ONE OF THE FACTORS THAT HELPED REALLY NAIL THAT DOWN AND THE EARLIEST ASSOCIATIONS WERE WITH NUMBER OF SEXUAL PARTNERS BUT AS YOU GOT MORE SPECIFIC AND COULD IDENTIFY HPV THE ODDS RATIOS GREW UP, BECAME HIGHER WITH CERVICAL CANCER. FINALLY THERE'S A LOT OF OCCUPATIONS THAT ARE HUMAN CARCINOGENS, AND THIS IS A POLITICALLY DIFFICULT AREA BECAUSE WHEN YOU IMPLICATE SOMETHING LIKE DIESEL IN LUNG CANCER, THERE ARE SUPPORTERS AND
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LOBBYING GROUPS THAT COMPLAIN TO CONGRESS, CONGRESS CALLS YOU IN AND WANTS YOU TO TESTIFY. THEY WANT YOUR DATA, SO THEY FILE FREEDOM OF INFORMATION ACT REQUEST, AND REQUEST YOUR DATA AND IMMEDIATELY REANALYZE TO PROVE YOU DID IT WRONG AND LOOKING AT THE DATA SOME OTHER WAY SHOWS DIESEL EXHAUST IS GOOD FOR YOU. SO IT'S REALLY IMPORTANT THAT YOU HAVE WELL-FUNDED GROUPS THAT INVESTIGATE PARTICULARLY THESE ENVIRONMENTAL AND OCCUPATIONAL CARCINOGENS. OKAY. WHAT CAN GO WRONG?
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AND FIRST I WANT TO JUST MENTION SOME ORDINARY CHALLENGES THAT EPIDEMIOLOGISTS FACE. ONE OF THEM IS THERE ARE SUBSTANTIAL GAPS IN WHAT WE UNDERSTAND ABOUT ENVIRONMENTAL EXPOSURES IN CANCER. SO SOME OF THOSE BIG INTERNATIONAL DIFFERENCES I SHOWED YOU WE DON'T UNDERSTAND. AND SO MORE WORK IS NEEDED. AND SOME EXPOSURES THOUGHT TO BE IMPORTANT ARE DIFFICULT OR IMPOSSIBLE TO ASSESS. AND SO I WILL TALK IN THE LAST SEGMENT OF THIS TALK ABOUT HOW WE GET AT SOME OF THOSE DIFFICULT EXPOSURES.
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HERE IS A FAVORITE DISEASE OF MINE, CHRONIC LYMPHOCYTIC LEUKEMIA, THE MOST COMMON ADULT ADULT LEUKEMIA IN THE WESTERN WORLD BUT WE DON'T UNDERSTAND EXTRINSICS CAUSE, THE BEST ETIOLOGIC FACTOR IS AGE AND HISTORY, AND 30 SNPS HAVE BEEN ASSOCIATED WITH CLL BUT WE DON'T HAVE A GREAT UNDERSTANDING OF WHAT THE EXTRINSIC SOURCES ARE. DIETARY RISK FACTORS REMAIN HIGHLY CONTROVERSIAL. THERE ARE A FEW THAT HAVE BEEN IMPLICATED, BUT IN GENERAL FOR A LOT OF CANCERS THAT WE'RE MOST
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INTERESTED IN WE REALLY HAVE NOT NAILED DOWN THE SPECIFIC DIETARY CAUSES. I'M GOING TO BRUSH BY DIET AGAIN IN A MINUTE AND GO INTO THIS. ONE STUDY WE DID IN OUR LARGE CASE CONTROL STUDY WAS ON MEAT CONSUMPTION. SO WE DID SHOW THAT INCREASING RATES OF MEAT CONSUMPTION, FRESH MEAT OR PROCESSED MEAT, WAS ASSOCIATED WITH INCREASING RATES OF LUNG CANCER, BUT I WOULD CAUTION YOU THAT THOSE STUDIES ARE FRAUGHT WITH DIFFICULTY, AND ONE REASON IS THAT IN OUR QUESTIONNAIRE WE IMAGINE THAT
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WE'RE ASKING PEOPLE PRECISELY ABOUT THEIR SOURCES OF MEAT CONSUMPTION, BUT IN FACT WHAT THEY ARE REALLY EATING ARE A COLLECTION OF OTHER ITEMS THAT MAY BIAS THE ASSESSMENT OF MEAT. AND SO FOR EXAMPLE FOOD QUESTIONNAIRES IS A MEAT OR NITRATES IN THE MEAT, IF THE HIGH FRUCTOSE CORN SYRUP IN THE BIG BOLUS OF SUGAR THEY ARE TAKING IN? WHAT ABOUT THE LOAD OF CARBOHYDRATES? WHAT ABOUT THE PROCESSED FOOD THAT'S IN THE BUN OR IN THE FRENCH FRIES? THE FAT, THE GLYPHOSPATE, OR
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MAYBE THE PERSON THAT JUST ATE ALL THIS IS NOT THE MOST HEALTH CONSCIOUS PERSON AND HAS OTHER UNMEASURED CONFOUNDERS THAT WERE NOT COVERED IN OUR STUDY. SO DIET IS A DIFFICULT AREA, ONE OF THE MORE CHALLENGING AREAS. WE HAVE A LOT LEFT TO DO IN THAT AREA. OKAY. OF COURSE EPIDEMIOLOGISTS HAVE DELVED INTO GENETICS, INCREASINGLY, AND ON THE GENETICS SIDES WE HAVE CHALLENGES AS WELL. ONE IS THAT MOST OF THE GENES IN GWAS STUDIES SINCE ABOUT 2007 ASSOCIATED WITH WITH COMMON
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CANCERS CONFER MINIMAL RISK, EXPLAIN ONLY A SMALL PORTION OF THE VARIATION. WHEN YOU PUT THEM IN RISK MODELS THEY HELP A LITTLE BIT BUT DON'T REALLY GIVE YOU THAT MUCH. HOW GENE AND ENVIRONMENT WORK TOGETHER IS REALLY POORLY UNDERSTOOD. SO YOU'LL SEE A LOT ABOUT GENE ENVIRONMENT, AND THE DREAM WITH GENE ENVIRONMENT IS THAT YOU HAVE A HIGH -- THAT A CERTAIN EXPOSURE IS ONLY WORKING IN THE PRESENCE OF CERTAIN GENES, AND IF YOU KNEW -- IF YOU COULD DEFINE THAT GENE-ENVIRONMENT
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INTERACTION REALLY WELL, ALL YOU'D HAVE TO DO IS INTERRUPT THE GENE OR INTERRUPT THE EXPOSURE AND YOU KNOCK OUT A BIG PORTION OF RISK. WELL, NICE IDEA BUT THERE ARE VERY FEW, IF ANY, PRACTICAL APPLICATIONS OF THAT. AGAIN, THERE COULD BE A WHOLE TALK ON GENE-ENVIRONMENT INTERACTION WHICH WON'T BE THIS TALK. FOR FAMILIES WE'VE STUDY FAMILIES FOR A NUMBER OF DECADES. AND USED THEM TO TRY TO IDENTIFY GENES BY CLASSICAL METHODS LIKE LINKAGE ANALYSIS, AND MORE RECENTLY EXON SEQUENCING, AND WE
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FOUND A FEW. BUT, AGAIN, IT'S DIFFICULT. SO ALL CANCER ON SOME LEVEL IS DUE TO GENETIC CHANGES BUT YOU HAVE TO SPES SPECIFY WHAT YOU MEAN BY GENETIC, GERMLINE OR SOMATIC CHANGES IN THE TUMOR, DO YOU MEAN POPULATION CHANGES WE DISCOVER IN GWAS OR DO YOU MEAN MAJOR GENES WE DISCOVER IN FAMILIES, AND DO YOU MEAN IDENTIFYING OUR FAVORITE CANDIDATE GENE AND LOOKING FOR THAT SPECIFICALLY, OR DO YOU MEAN THE AGNOSTIC SEARCH ACROSS THE WHOLE GENOME? SO HERE'S EXAMPLES OF OUR CANCER
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FAMILIES WHERE WE HAVE A GROUP OF LYMPHOPROLIFERATIVE MALIGNANCIES IN ONE KINDRED AND PERHAPS 50 OF THESE FAMILIES FOR CLL, AND THESE KINDS OF FAMILIES HAVE CLASSICALLY LED TO THE CLONING OF DIFFERENT TUMOR SUPPRESSOR GENES. WHEREAS IN POPULATION STUDIES, YOU HAD ONLY ABOUT FIVE YEARS AGO 240 DISEASE LOCI. I THINK THAT FIGURE NOW IN 2017 IS CLOSE TO 7,000. STILL, THOSE GENES EXPLAIN A SMALL COMPONENT OF RISK. SO, I'LL MENTION OUR STUDY, EAGLE, AGAIN QUICKLY. WE DID A CASE CONTROL STUDY OF
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LUNG CANCER DRIVEN BY THE IDEA THAT IN SPITE OF THE FACT WE UNDERSTAND A LOT ABOUT OF CAUSE OF LUNG CANCER, WHICH IS SMOKING, IT'S STILL THE LEADING CAUSE OF CANCER MORTALITY IN THE UNITED STATES. AND TREATMENT AND SCREENING OF BOTH POSE VERY, VERY SIGNIFICANT CHALLENGES. SO IT WAS TEN YEARS AGO WE FIELDED EAGLE. THIS CASE-CONTROL STUDY OF 2,000 CASES AND 2,000 CONTROLS. ONE OF THE FIRST THINGS WE SHOWED WAS THAT FAMILY HISTORY WAS A RISK FACTOR. SO WE WANTED TO IDENTIFY THE
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GENES, AFTER YOU ADJUST FOR PRETTY OF EVERY OTHER KNOWN LUNG CANCER RISK FACTOR. ONE OF THE FEATURES OF THIS STUDY IS THAT WE LIKE TO SAY IT WAS A MOLECULAR OR INTEGRATIVE EPIDEMIOLOGY STUDY. ORIGINALLY WHAT EPIDEMIOLOGY IT WOULD IDENTIFY RISK FACTOR BY A QUESTIONNAIRE, AND RELATE IT TO AN OUTCOME LIKE A CANCER. AND USE STATISTICAL TECHNIQUES TO RELATE THE EXPOSURE IN DISEASE. ON THE BASIS OF SHOWING THE CORRELATION OR SOME MEASURE OF STATISTICAL ASSOCIATION INFER
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THAT, OH YES, TOBACCO IS A RISK FACTOR. WELL, THE IDEA OF MOLECULAR EPIDEMIOLOGY IS THAT YOU WOULD ALSO MEASURE BIOMARKERS. AND SO BY MEASURING BIOMARKERS, YOU CAN GAIN AN ADDITIONAL AMOUNT OF EVIDENCE. SO MAYBE WE WOULD MEASURE A TOBACCO MARKER IN THE BLOOD, INTERNAL DOSE, AND KNOW THE INTERNAL DOSE OF TOBACCO. OR MAYBE WE WOULD MEASURE A DNAED A ADDUCT OR POLY CYCLIC ADDUCT AND GATHER OR INFORM CERTAIN EVIDENCE OF SEQUENCE OF CAUSATION SO ADDING BIOMARKERS TO INVESTIGATE GENES AND MECHANISMS.
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AND THEN MORE RECENTLY INTEGRATIVE EPIDEMIOLOGY, THE IDEA THAT WE CAN LEARN EVEN MORE BY LOOKING AT THE BEHAVIORS THAT ARE RELATED TO EXPOSURE, AND BY LOOKING AT OUTCOMES WE CAN UNDERSTAND SOMETHING ABOUT THE FACTORS THAT MAKE SOMEBODY HAVE A GOOD OR BAD PROGNOSIS OR GOOD OR BAD OUTCOME. SO IN OUR CASE CONTROL STUDY WE ACTUALLY GOT LIQUID NITROGEN CANISTERS INTO A NUMBER OF OUR HOSPITALS AND WOULD SIT THERE AND WAIT FOR THE SURGEON TO RESECT THE TUMOR AND THEN THE PATH OLOGIST WOULD TAKE THE
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TUMOR AND CUT PIECES AND WE'D HAVE A PIECE OF PAPER AND MARK WHERE THEY CAME FROM AND GET PIECES OF TUMOR TO CONDUCT THESE KINDS OF STUDIES. WE ALSO HAD A REFINED QUESTIONNAIRE, SO IN ADDITION TO ASKING PEOPLE WHAT THEY ATE WE WOULD ASSESS THINGS LIKE DONENESS, SO CERTAIN CARCINOGENS LIKE HETEROCYCLIC AMINES ARE RELATED, COOKED OR MORE RARE COULD BE RELATED TO LEVELS OF THOSE CARCINOGENS. HERE ARE SOME INSTRUMENTS WE INCLUDED ON THE BEHAVIOR SIDE. THE FAGORSTROM TEST FOR NICOTINE
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DEPENDENCY QUESTIONNAIRES RELATED TO ANXIETY, DEPRESSION, PERSONALITY AND OTHER FACTORS. SO WHAT HAS MOLECULAR EPIDEMIOLOGY CONTRIBUTED? FOR EXAMPLE, WE UNDERSTAND IN PART BASED ON BIOMARKER STUDIES HPV IS THE CAUSE OF 100% OF CERVICAL CANCER AND PREVENTION IS THEREFORE POSSIBLE WITH THE VACCINE. WE UNDERSTAND THAT CUTTING DOWN ON SMOKING IS INEFFECTIVE IN TERMS OF REDUCING RATE OF CANCER BECAUSE YOU COMPENSATE BY THE MANNER IN WHICH YOU INHALE. AND SO BIOMARKER STUDIES SHOW
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THAT LEVELS OF CARCINOGENS DON'T DECLINE. AND GWAS STUDIES HAVE BEEN PERFORMED FOR HUNDREDS OF CONDITIONS BASED ON BIOMARKER STUDIES. THIS COULD BE A WHOLE LECTURE. CONSORTIA ARE COMMONLY USED IN EPIDEMIOLOGIC STUDIES AND GROUPS HAVE SPRUNG UP TO EXPAND DATA COLLECTION AND REDUCE MISCLASSIFICATION BY USING SPECIALIZED INSTRUMENTS IN THOSE STUDIES. OKAY. SO I'M GOING TO COVER THE LAST TWO SECTIONS RAPIDLY. WHAT CAN GO WRONG? I'M REMINDED OF THE CLASSICAL WORK ON THE STRUCTURE OF
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SCIENTIFIC REVOLUTIONS, AND THIS WORK POINTS OUT THAT OUR UNDERSTANDING OF SCIENTIFIC PARADIGMS DOESN'T CHANGE IN A CONTINUOUS MANNER BUT TENDS TO BE DISCONTINUOUS. THE WAY KUHN DESCRIBED IT BASICALLY MODELS HAVE TO BE OVERTURNED. SO REALLY WHAT HAPPENS IS THE ADVOCATES FOR CERTAIN WAYS OF THINKING HAVE TO DIE BEFORE ANYTHING CHANGES. NOW A LOT OF US ARE SKEPTICAL ABOUT THAT. WE THINK I'M NOT ATTACHED TO MY HYPOTHESIS. AND THE MOMENT SOMETHING NEW COMES OUT I'M GOING TO LOOK AT
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THE EVIDENCE OBJECTIVELY AND ADOPT IT. IN FACT THAT'S NOT WHAT HAPPENS IN PRACTICE. LET ME GIVE YOU THE EXAMPLE OF OBESITY. OBESITY IS STRIKINGLY INCREASING IN THE UNITED STATES. IT'S ALSO STRIKINGLY INCREASING WORLDWIDE. COUNTRIES, THE RATES ARE RISING. THIS IS OVERWEIGHT. THIS IS OBESITY. 53% OF THE ADULT ADULT POPULATION IN THE UNITED STATES, 21% IS OBESE. ALL YOU HAVE TO DO IS WALK INTO A WALMART AND SEE THE CARTS, AND YOU GET AN IDEA. WHY ARE WE CONCERNED IN CANCER?
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WELL, BEING OVERWEIGHT IS ASSOCIATED WITH 13 KINDS OF CANCER. WHAT CAUSED THIS? ONE WAY TO TRACE THIS BACK TO THE CAUSE IS ANSIL KEYS, THE GUY THAT INVENTED K-RATIONS, HE DID THE EARLIEST DIETARY INTERVENTION STUDIES FASCINATING TO READ TODAY. ONE THING HE DID WAS A MULTI-COUNTRY STUDY WHERE HE FOUND AN ASSOCIATION BETWEEN SATURATED FAT AND CARDIOVASCULAR DISEASE. AND THIS LED TO RECOMMENDATIONS TO EAT LESS FAT, WHICH IF YOU HAVE THREE MACRONUTRIENTS, FAT, CARBOHYDRATES AND PROTEIN,
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YOU'RE INVARIABLY GOING TO INCREASE THE AMOUNT OF CARBOHYDRATE IN THE DIET. SO THIS LED TO USDA RECOMMENDATIONS, TO EAT LESS FAT, AND EAT MORE CARBOHYDRATES. AND THIS LED TO INSTITUTIONS ADOPTING THESE RECOMMENDATIONS WHICH ARE STILL TO SOME DEGREE ADOPTED TODAY BY THE AMERICAN DIABETES ASSOCIATION, AMERICAN HEART FOUNDATION, ET CETERA. AMERICAN PUBLIC DID FOLLOW RECOMMENDATION, SATURATED FAT WENT DOWN, CARB WENT UP. WHAT WAS THE RESULT? WELL, HERE IS AN OBESEOGENIC DIET GIVEN TO FATTEN RATS.
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OUR DIET OF 40% REFINED CARBOHYDRATES AND 40% OIL, WHICH IS A DOUGHNUT, IS EXACTLY WHAT'S GIVEN TO RATS. AND IT'S WHAT'S CURRENTLY THE STANDARD AMERICAN DIET. AND THIS HAS RESULTED IN A STARK INCREASE IN OBESITY AND OVERWEIGHT. HOWEVER, WHEN YOU DO RANDOMIZED CLINICAL TRIALS TO LOOK AT THE EFFECT OF REDUCING SATURATED FAT, GENERALLY THESE MULTI-MILLION DOLLAR STUDIES HAVE COME UP EMPTY. SO THERE'S BEEN NO DIFFERENCE PRETTY MUCH WITH A FEW EXCEPTIONS IN CARDIOVASCULAR
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EVENTS, ESPECIALLY IN MORTALITY. SO THIS INTERVENTION HAS NOT BEEN PARTICULARLY HELPFUL. AND THERE'S A VAST LITERATURE ON THIS NOW. HOWEVER, WHAT HAS HAPPENED IS THAT DIABETES IN THE UNITED STATES HAS STEADILY INCREASED. AND IF YOU LOOK AT DIABETES PREVALENCE, THIS IS 2012, UP TO 20%, EVEN MORE, OF THE ADULT POPULATION ACROSS THE OBESITY BELT PARTICULARLY HAS DIABETES. AND A MUCH HIGHER PROPORTION HAVE PREDIABETES. SO WHAT'S THE CAUSE? WELL, DIETARY CHANGES HAVE TO BE NUMBER ONE.
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WE COULD GIVE A WHOLE TALK ON THE TOPIC OF LATE AT NIGHT BUT THE IDEA OF DECREASING LIGHT EXPOSURE MAY HAVE SOMETHING TO DO WITH OBESITY. THERE'S A VARIETY OF OTHER CAUSES. I DON'T HAVE TIME TO GO INTO THESE BUT PROCESSED FOODS, INCREASING INTAKE OF NUTRITIONALLY EMPTY FOODS, A LESS ACTIVE POPULATION, OBESOGENIC, PEOPLE CAN ONLY ACCORD THIS FOOD AND LATE NIGHT COOKING I DON'T HAVE TIME TO GO INTO LATE AT NIGHT BUT THERE'S SOME EVIDENCE THAT LIGHT POLLUTION AT NIGHT AND LESS
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EXPOSURE TO LIGHT DURING THE DAY DISRUPTS CIRCADIAN RHYTHM, THE FIRST EFFECT IS WEIGHT GAIN. SO BEFORE WE DEVELOPED DIABETES WE DEVELOPED INSULIN RESISTANCE FOR MANY DECADES. AND INSULIN RESISTANCE IS ASSOCIATED WITH A VARIETY OF BAD ENDPOINTS LIKE ALZHEIMER'S. OVERALL MORTALITY, AND CANCER MORTALITY. SO THIS IS AN AREA OF CURRENT RESEARCH RIGHT NOW. OKAY. THAT'S ALL I CAN SAY ABOUT THAT. I WILL TAKE TWO MINUTES TO TALK ABOUT WHAT'S NEXT. TECHNOLOGY. SO WE USE TECHNOLOGY TO CAPTURE
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SOME EXPOSURES THAT HAVE PREVIOUSLY BEEN INACCESSIBLE. WE COULD IMPROVE MISCLASSIFICATION. IT'S CRITICAL TO VALIDATE THESE. WHAT CAN WE GET AT THAT WE COULDN'T BEFORE? EXAMPLES ARE SLEEP, PHYSICAL ACTIVITY, VITAL SIGNS, CIRCADIAN VARIATION, SOCIAL FACTORS, LOCATION, WHERE YOU ARE, AND PULSE OXIMETRY, RELATIVE TO LUNG CANCER. SLEEP, MANY OF YOU HAVE FIT BIT OR WATCH, YOU CAN QUANTITATE THE STAGES. SLEEP IS RELATED TO OBESITY. DATA FROM NHANES, IF YOU SLEEP LESS THAN SIX HOURS PER NIGHT
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YOUR RATE OF ADDICTION GOES UP, RATE OF DIABETES GOES UP. PHYSICAL ACTIVITY LIKEWISE CAN BE TRACKED BY ACTIGRAPHY. VITAL VINES, VERY IMPORTANT. I DON'T HAVE TIME TO GO INTO IT. WHERE FOCUSING A LOT OF EFFORT ON CIRCADIAN VARIATION. SOCIAL DATA, WHO YOU HANG OUT WITH IS VERY, VERY IMPORTANT IN TERMS OF A LOT OF TRAITS. FINALLY PULSE OX, AS MOST OF YOU PROBABLY ARE AWARE, YOU CAN JUST PUT YOUR FINGER ON YOUR PHONE AND GET YOUR PULSE OX. PULSE OX IS RELATED TO ALL-CAUSE
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MORTALITY, SO IT CAN BE TRACKED EASILY IN COHORTS. ALL OF THIS DATA, EPIDEMIOLOGIC DATA, GENES, BIOMARKERS AND TECHNOLOGY, IS WHAT WE THINK WILL EVENTUALLY CREATE FUTURE IMPROVED RISK MODELS. SO I THINK THIS PROBABLY IS A GOOD PLACE TO STOP. I'M LEAVING LESS TIME THAN I HOPED I WOULD BUT I'M HAPPY IF THERE ARE A FEW QUESTIONS. THANK YOU. YES? >> (INAUDIBLE). >> SO E-CIGARETTES ARE BEING TRACKED IN THE PATH STUDY. AND NEWER STUDIES WILL TRY TO FOLLOW THEM BUT MOST OF THE
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CLASSIC COHORTS, ONE OF THE PROBLEMS IS HAVING TO WAIT TWO DECADES FOR PEOPLE TO GET DIFFERENT DISEASES. THERE ARE NO QUESTIONS IN PLCO OR AARP OR ANY COHORTS ON E-CIGARETTES. AND THE PROBLEM WITH DOING CASE CONTROL STUDIES WHERE YOU CAN LOOK AT RAPIDLY EMERGING RISK FACTORS IS THAT IT TAKES A WHILE FOR THEM TO HAVE HEALTH END POINTS, SO IT'S GOING TO BE SOME TIME BEFORE WE HAVE GOOD HUMAN EPIDEMIOLOGY DATA. WHAT WE WILL HAVE THOUGH IS MOLECULAR EPIDEMIOLOGY DATA.
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WE WILL HAVE BIOMARKER DATA FROM PATH. AND SOME OTHER STUDIES LIKE PATH, THAT GIVE QUESTIONNAIRES TO YOUNG PEOPLE AND THE ONES THAT ARE USING E-CIGARETTES WE'LL HAVE BIOMARKER STUDIES ON THEM IN THE NEXT YEAR OR TWO. YES? >> (INAUDIBLE). >> SO -- SORRY, IT WASN'T POLY CYCLIC, IT WAS HETEROCYCLIC AMINES, THOSE ARE SPECIFIC -- WHAT'S BEST STUDIED IS MEAT. WHETHER OTHER PROTEINS FORM THEM, I DON'T THINK THEY DO. IT'S REALLY AN ISSUE WITH VARIOUS KINDS OF MEAT. AND THE LATEST STUDIES -- EVEN
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THOSE THESE ARE ESTABLISHED CARCINOGENS, NOT SHOW BIG RISKS ASSOCIATED WITH DONENESS OR THE HETEROCYCLIC AMINES. IT WAS A BIG THING FIVE OR TEN YEARS AGO, IT'S NOT EMERGED AS A DRAMATIC RISK FACTOR LATELY. I PUT MY E-MAIL ON THE FRONT PAGE. YOU HAVE ANY QUESTIONS THAT WE DIDN'T GET TO GO IN, I REALIZE I COVERED A WIDE VARIETY, NOT VERY DEEP, SO IF YOU HAVE QUESTIONS PLEASE DO E-MAIL ME AND I'LL TRY TO GET BACK AT YOU. FOR ANNOUNCEMENTS, WE'RE DOING OUR PATHOLOGY TOUR TODAY AT 6:00.
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SO FOR THOSE OF YOU WHO WANT TO GO SEE THE PATHOLOGY FACILITY IN BUILDING 10, WE'LL BE MEETING OUT IN THE HALLWAY AT THE END OF THE LECTURE. SO OUR NEXT SPEAKER IS DR. RYAN, SHE GOT HER UNDERGRADUATE TRAINING IN IRELAND, Ph.D. AT THE UNIVERSITY COLLEGE OF DUBLIN, AND THEN IN 2006 JOINED THE NCI CANCER PREVENTION FELLOWSHIP PROGRAM, AND SHE THEN WORKED AS A POSTDOCTORAL FELLOW IN KURT FARRIS' LAB AND SHE'S NOW AT NCI EARL STATMAN SENIOR TRACK INVESTIGATOR. SHE INJURED HER LEG SO SHE WILL
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HAVE TO SIT DOWN DURING THE LECTURE. BE KIND TO HER. >> MY APOLOGIES FOR THAT. OKAY. OKAY. SO MY NAME IS BRIE RYAN, AN INVESTIGATOR HERE AT NCI. I DID MY POSTDOC HERE, I'VE BEEN HERE FIVE, TEN YEARS NOW. MY LAB STUDIES LUNG CANCER, SPECIFICALLY LUNG CANCER HEALTH DISPARITIES. A LOT OF THE TALK TODAY YOU'LL SEE SOME EXAMPLES OF LUNG CANCER BUT THIS IS A TALK ABOUT A BROADER CONTENTION SIMILAR TO WHAT NEIL WAS TALKING ABOUT IN TERMS OF CANCER HEALTH DISPARITIES. WE'LL TOUCH ON DIFFERENT THEMES,
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NOT ALL CANCER SPECIFIC. IF YOU TOUCH ON SOMETHING YOU WANT MORE INFORMATION OR OR IF YOU WANT TO FOLLOW UP QUESTIONS, E-MAIL ADDRESS IS ON THE FRONT AND I WORK IN BUILDING 37. I'M GOING TO TALK ABOUT KEY -- JUST GIVE YOU AN OVERVIEW OF WHAT CANCER HEALTH DISPARITIES IN THE U.S. LOOK LIKE AT THE MOMENT. THE SECOND PART WE'RE GOING TO TALK A LITTLE BIT ABOUT SOME OF THE KEY FACTORS THAT CONTRIBUTE TO DISPARITIES. AND THEN THE THIRD PART BRIEFLY WE'RE GOING TO TALK ABOUT WHERE
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WE ARE RIGHT NOW AND WHAT THE FUTURE FOCUSES ARE IN THIS AREA. ALL RIGHT. I'M GOING TO START WITH A COUPLE DEFINITIONS, A COUPLE SLIDES, SO BEAR WITH US. THROUGHOUT THE TALK I OFTEN MENTION THINGS LIKE RACIAL DISPARITIES OR ETHIC DISPARITIES. IT'S IMPORTANT TO DEFINE AND KNOW BOTH ARE IMPORTANT IN THIS TYPE OF RESEARCH. WHEN WE USE THE TERM RACE WE'RE REFERRING TO BIOLOGICAL DIFFERENCES BETWEEN GROUPS, ASSUMED TO HAVE DIFFERENT BIOGEOGRAPHICAL ANCESTRY OR GENETIC MAKEUP.
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ETHNICITY, WHILE RELATED, IS DISTINCT. HERE WHAT WE'RE TALKING ABOUT IS A MULTI-DIMENSIONAL CONSTRUCT, REFLECTING BIOLOGICAL FACTORS, GEOGRAPHICAL ORIGINALS IN, HISTORICAL INFLUENCE, SHARED BELIEVES AND CUSTOMS THAT MAY OR MAY NOT HAVE A COMMON GENETIC ORIGIN. BOTH ARE IMPORTANT IN STUDYING DISPARITIES RESEARCH. SO I MENTIONED ONE OF THE FIRST THINGS WANT TO DO IS GIVE YOU A LOOK AT DISPARITIES IN THE U.S. ON THE LEFT YOU CAN SEE DIFFERENCES IN LIFE EXPECTANCY IN THE UNITED STATES,
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SPECIFICALLY JUST BASED ON RACE. AND THE FIRST THING YOU SHOULD HOPEFULLY APPRECIATE IS FOR MEN AND WOMEN IN GENERAL BLACK MEN ARE EXPECTED TO LIVE 6 1/2 YEARS SHORTER, BLACK WOMEN 5 YEARS. THAT'S A SIGNIFICANT DISCREPANCY IN LIFE EXPECTANCY. YES, CARDIOVASCULAR DISEASE CONTRIBUTES A BIT TO DIFFERENTIAL LIFE EXPECTANCY, CANCER ALSO PLAYS A VERY IMPORTANT ROLE IN THIS. CANCER HEALTH DISPARITIES ARE THE TOPIC OF THE PRESENTATION TODAY. ALL RIGHT. AGAIN, DEFINITIONS HERE TODAY,
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SO YOU KNOW HOW THE NCI DEFINES CANCER HEALTH DISPARITIES, IT'S DIFFERENCES IN THE INCIDENCE, PREVALENCE MORTALITY AND BURDEN OF CANCER AND/OR RELATED HEALTH OUTCOMES THAT EXIST AMONG SPECIFIC POPULATIONS WITHIN THE UNITED STATES. SPECIFICALLY THE NCI AND INDEED MANY OTHER ORGANIZATIONS HAVE NOTED THAT AFRICAN-AMERICANS HAVE THE HIGHEST DEATH RATES FROM ALL LUNG CANCERS COMBINED, INCLUDING MALIGNANCY OF LUNG, COLON RECTUM BREAST PROSTATE AND CERVIX, OF ALL RACIAL GROUPS IN THE UNITED STATES.
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THAT GIVES YOU A SENSE OF THE BURDEN AND SCOPE OF THE PROGRAM. THIS IS LOOKING AT MEN FROM THE CDC, INCIDENCE OF CANCER BY RACE AND ETHNIC GROUPS OVER A PERIOD OF TIME, THIS GOES BACK TO 1999. YOU CAN SEE OUT OF ALL GROUPS IN THE UNITED STATES BLACK MEN, ALSO WOMEN, HAVE THE HIGH'S MORTALITY. SORRY, HIGHEST INCIDENCE, EXCUSE ME. IN ADDITION IT'S NOT JUST THAT THE INCIDENCE IS HIGHER. WHAT A LOT OF STUDIES HAVE NOW SHOWN IS IN GENERAL THE AGE AT WHICH THE CANCER IS DIAGNOSED IS ALSO EARLIER.
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SO WHAT'S GRAPHED ON THIS, WHAT'S SHOWN HERE ACTUALLY, IS FROM COLLEAGUES OF OURS IN DCEG WHERE NEIL JUST PRESENTED. ON THE RIGHT-HAND SIDE AFRICAN-AMERICANS ARE EXPECTED TO BE DIAGNOSED AT A LATER AGE, BUT YOU CAN SEE MAJORITY OF CANCERS INCLUDING LUNG ARE MORE LIKELY TO BE DIAGNOSED AT AN EARLIER AGE IN AFRICAN-AMERICANS COMPARED TO EUROPEAN-AMERICANS. IT'S NOT JUST A HIGHER BURDEN, IT'S THAT THE ACTUAL INCIDENCE IS ALSO DIAGNOSED AT EARLIER TIME IN THEIR LIFE. SO WHAT ARE THE REASONS FOR
1:03:46
THIS? SEVERAL REASONS WERE PROPOSED IN THE PAPER. ONE IS ETIOLOGIC HETEROGENEITY. WE KNOW CAUSE OF CANCER CAN VARY ACROSS VARIOUS GROUPS. AND SO IN THAT CASE THE CANCER CAN OCCUR AT A DIFFERENT AGE. IN ADDITION, IT COULD BE RELATED TO THE TIMING OF THE -- OR INTENSITY OF THE EXPOSURE. SO ONE EXAMPLE HERE COULD BE HPV EXPOSURE, IF YOU'RE EXPOSED EARLIER, DISEASE IS MORE LIKELY TO OCCUR EARLIER, OR SAME CAN TOBACCO, IF YOU START SMOKING EARLY YOU ONE MIGHT IMAGINE YOU'RE DIAGNOSED WITH CANCER
1:04:22
EARLIER. OTHER POSSIBILITIES WE'LL TOUCH ON LATER LOOKING AT THE TIMING AND PRESENCE AND FREQUENCY OF EARLY DETECTION AND TALK A LITTLE BIT ABOUT THAT. BECAUSE OF THIS VERY STRONG OBSERVATION THAT MANY CANCERS ARE IN FACT DIAGNOSED AT AN EARLIER AGE AMONGST AFRICAN-AMERICANS, THE NCI HAS ORGANIZED EARLY ONSET MALIGNANCY INITIATIVE WORKING THROUGHOUT THE UNITED STATES TO STUDY THIS IN MORE DETAIL, CAN WE UNDERSTAND WHY THESE DISPARITIES OCCUR, AND UNDERSTANDING IT WHAT
1:04:50
CAN WE ACTUALLY DO TO INTERVENE. SOMETHING THAT'S ALSO BEEN STUDIED QUITE -- AN AREA THAT'S BEEN STUDIED SOMEWHAT MORE, AGAIN BY SOME COLLEAGUES IN DCEG, INCLUDING LINDSEY MORTON, THIS IDEA OF SECOND CANCERS. A LOT OF STUDIES ARE LOOKING AT PRIMARY CANCER, FIRST INCIDENCE OF CANCER. OF LATE PEOPLE HAVE BEEN ASKING THE QUESTION WHAT ABOUT SECOND PRIMARIES? AS WE HAVE MORE AND MORE CANCER SURVIVORS, WHICH IS A GOOD THING, IT'S ALSO THE FIELD OF CANCER SURVIVORSHIP THAT'S VERY
1:05:26
IMPORTANT BECAUSE WE NEED TO FOLLOW THOSE POPULATIONS AND TRY AND UNDERSTAND WHAT IS THEIR SURVIVORSHIP LIKE, ARE THEY AT RISK FOR SECOND CANCERS? A LOT OF TREATMENTS FOR CANCER INCLUDE RADIATION, AND RADIATION ITSELF IS A RISK FACTOR FOR CANCER. SOME OF THE STUDIES THAT HAVE BEEN CONDUCTED, THIS IS ONE EXAMPLE BY -- HER NAME IS -- IT'S OUT OF MY HEAD AT THE MOMENT. WHAT THEY FOUND, ENDOMETRIAL CANCER, FOLLOWING SURVIVORS, THEY LOOKED TO SEE INCIDENCE OF SECOND CANCER.
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IN THAT EXAMPLE THERE AGAIN THEY ALSO FOUND DISPARITIES. SO OVERALL IF THEY LOOKED AT EVERY CANCER SITE YOU CAN SEE THE STANDARD INCIDENCE RATE WAS 20%, 20% INCREASED INCIDENCE RATE OF ALL CANCER TYPES, IN THE BLACK PARTICIPANTS, BUT IT WAS IN FACT EVEN LESS IN THE WHITES. MORE WORK NEEDS TO BE DONE IN THIS AREA BUT THE STUDY POINTS TO IMPORTANCE OF STUDYING CANCER HEALTH DISPARITIES IN THE CONTEXT OF PRIMARY CANCER AND ALSO WITHIN THE CONTEXT OF SECONDARY TUMORS AS WELL.
1:06:33
SO WE TALKED A LITTLE BIT ABOUT INCIDENCE RATES BUT WHAT ABOUT MORTALITY? SO HERE AGAIN SHOWN FOR BOTH MEN AND WOMEN ARE DATA FROM THE CDC SHOWING THE MORTALITY FROM CANCER, FROM BOTH MEN AND WOMEN, IS ALSO MUCH HIGHER COMPARED TO ALL OTHER RACIAL/ETHNIC GROUPS IN THE UNITED STATES. SO LOOKING AT THIS A LITTLE BIT CLOSER, THIS IS DATA FROM ONCOLOGY FOCUSING ON THE FOUR MAIN TYPES OF CANCER. BREAST, PROSTATE, LUNG AND COLORECTAL. YOU CAN GET A SENSE OF WHAT THE DEGREE OF THE DISPARITY LOOKS
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LIKE. IT'S NOT JUST HIGHER BUT HOW MUCH HIGHER IS IT. AND YOU CAN SEE THAT FOR PROSTATE AND BREAST CANCER THE DIFFERENCE IN MORTALITY BETWEEN EUROPEAN-AMERICANS AND AFRICAN-AMERICANS IS QUITE HIGH. NOW IT'S IMPORTANT TO EMPHASIZE THAT OFTENTIMES WE DO THESE STUDIES TO LOOK AT A SNAPSHOT, ONE MEASURE AT A PARTICULAR TIME. WHAT'S EQUALLY IMPORTANT IS TO SEE TWO ENDS CHANGE OVER TIME. IN SOME WORK NEIL DESCRIBED HE TOOK YOU THROUGH SOME OF THIS. THIS IS WHAT'S DONE IN THE TYPE
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OF ANALYSIS DONE HERE, THIS IS LOOKING AT THE MORTALITY OF PATIENTS WITH PROSTATE CANCER, BROKEN DOWN BY WHETHER PARTICIPANTS ARE WHITE, BLACK OR ASIAN. IT LOOKS OVER TIME, ARE WE DOING ANY BETTER? YOU CAN SEE COMPARED TO PEOPLE WHO ARE DIAGNOSED BETWEEN 1990 AND 1994 TO THOSE IN 2005-2009, THE LIKELIHOOD THEY SURVIVE IS MUCH BETTER. FOR BLACK PATIENTS IT'S IMPROVING EVEN MORE, A GOOD TREND. HOWEVER THERE IS DATA FROM BREAST CANCER SUGGESTING WE'RE SEEING THE OPPOSITE TREND.
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IN ADDITION THE POINT OF THIS SLIDE IS TO SAY YES IT'S IMPORTANT TO LOOK AT WHAT'S HAPPENING RIGHT NOW, BUT PERHAPS ALSO EQUALLY AS IMPORTANT IS TO LOOK AT HOW TRENDS VARY OVER TIME BECAUSE IT CAN ALSO PORTEND AN EMERGING DISPARITY THAT YOU MIGHT WANT TO LOOK AT AND THAT YOU MIGHT WANT TO ADDRESS. OKAY. SO JUST LIKE NEIL HAD GONE THROUGH IN HIS TALK, MANY TOPICS ARE VERY BROAD. I COULD GIVE YOU A WHOLE TALK JUST ON ONE OF THESE FACTORS, YOU KNOW, ONE OF FIVE FACTORS, VERY COMPLEX.
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THE GOAL REALLY OF THE PRESENTATION TODAY IS TO GIVE YOU A SENSE FOR THE MULTI-FACTORIAL NATURE OF THE PROBLEM. AND BEING MULTI-FACTORIAL THERE ARE MANY DISCIPLINES THAT ARE REQUIRED TO TRY TO GET A BETTER PICTURE OF WHAT'S GOING ON. I'VE BROKEN IT INTO FOUR. IT COULD BE MANY MORE GROUPS, BUT AT ONE LEVEL THE AREAS I FOCUS ON IS ON GENETICS, THAT'S MY BACKGROUND, I'LL TALK ABOUT THAT LATER ON. YOU CANNOT GIVE A TALK ABOUT CANCER HEALTH DISPARITIES WITHOUT ACKNOWLEDGING THE HUGE
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IMPORTANCE OF ACCESS TO CARE WHICH WE'RE GOING TO DISCUSS, IMPORTANCE OF EXPOSURE AND LIFESTYLE FACTORS, AND SOCIAL DETERMINANTS. AND THE IDEA IS OF COURSE THAT EACH OF THESE FACTORS DON'T OPERATE ALONE. THEY ALL INTERACT TOGETHER. AND SO WHILE I MYSELF MAY NOT STUDY EACH OF THESE INDIVIDUAL FACTORS, ALL THE RESEARCH THAT WE DO TO KEEP YOU AWARE ALL THESE ARE IMPORTANT, IT'S IMPORTANT TO SHARE COLLEAGUES FOR POSSIBLE LOOK FOR SYNERGY WITHIN THEM. SO IN TERMS OF FACTORS THAT
1:10:05
COULD CONTRIBUTE TO DISPARITIES, AT A VERY SORT OF HIGH LEVEL PICTURE, THE FIRST THING TO NOTE IS GEOGRAPHY MATTERS. WHY DOES GEOGRAPHY MATTER? THIS IS A PICTURE OF THE UNITED STATES, BROKEN DOWN BY STATE. WHAT IT SHOWS IS FOR ALL CANCERS COMBINED, JUST THE FACT THAT DEPENDING ON WHERE YOU LIVE AS YOU CAN SEE THE PALE COLORS ARE LOW INCIDENCE OF CANCER WHERE THE MORE INTENSE BLUE COLORS REFLECT HIGHER INCIDENCE. JUST BASED ON GEOGRAPHY WITHIN IS THERE'S A VERY LARGE DIFFERENCE IN THE INCIDENCE
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RATES OF ALL CANCERS. THERE ARE MANY DIFFERENT FACTORS THAT CAN CONTRIBUTE TO THIS BUT GEOGRAPHY MATTERS IS THE POINT. SO WHY DOES IT MATTER AND HOW COULD IT MATTER? A FEW THINGS TO MENTION IS THAT AGAIN YOU COULD GIVE AN ENTIRE TALK JUST ON HOW SOCIOECONOMIC STATUS CONTRIBUTES TO DISPARITIES BUT IT'S A HUGELY IMPORTANT FACTOR. WE KNOW, FOR EXAMPLE, THAT A LOW SOCIOECONOMIC STATUS NEIGHBORHOOD IN ADDITION TO ITSELF BEING A RISK FACTOR FOR MANY TYPES OF CANCER INCLUDING
1:11:13
LUNG, IT ALSO CONFERS A RISK BEYOND AN INDIVIDUAL SOCIOECONOMIC STATUS. IT MEANS THE NEIGHBORHOOD ONE LIVES IN IS AN IMPORTANT DETERMINANT OF CANCER INCIDENCE MORE THAN JUST YOUR INDIVIDUAL SOCIOECONOMIC STATUS. AND THAT'S IMPORTANT. HOW DOES IT DO THAT? OF COURSE, POLLUTION AGAIN AS NEIL TALKED ABOUT IN HIS SEMINAR IS KEY CAUSE OF CANCER DISPARITIES, AND IT'S KNOWN IN CERTAIN COMMUNITIES THAT HAVE HIGHER REPRESENTATION OF AFRICAN-AMERICANS WITHIN THEM THOSE AREAS ALSO EXPERIENCE
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HIGHER BURDEN OF POLLUTION. THESE ARE ALL IMPORTANT FACTORS. DEPENDING ON WHERE YOU LIVE, YOU MAY ALSO HAVE DECREASED ACCESS TO PREVENTION OF SERVICES. THESE ARE THINGS AS SIMPLE AS SMOKING CESSATION SERVICES. SMOKING, THE DECREASES WE'VE SEEN IN CANCER INCIDENCE OVER THE PAST NUMBER OF DECADES, ARE HUGELY DUE TO DECLINE IN SMOKING IN THE UNITED STATES. SMOKING CESSATION HAS BEEN AND CONTINUES TO BE THE NUMBER ONE THING WE CAN DO TO DECREASE PREVALENCE OF CANCER. DEPENDING ON WHERE YOU LIVE, YOU
1:12:16
MAY HAVE MORE OR LESS ACCESS TO THE TYPES OF SERVICES. IF YOU ARE MORE LIKELY TO LIVER WHERE HAVE YOU ACCESS TO HEALTH CLINICS OR WHAT WE CALL PRIMARY CARE PHYSICIAN, FOR EXAMPLE, AT THOSE VISITS THEY ASK DO YOU SMOKE. IF YOU SAID I SMOKE, THEY WILL SAY YOU SHOULD STOP SMOKING, HERE ARE SOME SERVICES WHERE I CAN HELP YOU DO THAT. ACCESS TO RESOURCES IS NOT UNIFORM ACROSS THE UNITED STATES. WE'LL TALK ABOUT RURAL AND URBAN DISPARITIES BUT THEY ARE REAL FACTORS THAT CAN CONTRIBUTE TO
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AN INDIVIDUAL'S HEALTH BEHAVIORS BUT ALSO OVERALL HEALTH THEMSELVES. IN RECENT YEARS, ESPECIALLY IN THE LAST 12 TO 18 MONTHS, THIS IDEA OF STUDYING AND CONTINUING TO STUDY IN MORE DETAIL RURAL AND URBAN HEALTH DISPARITIES HAS REALLY TAKEN HOLD. OF COURSE, IT'S BEEN AN AREA THAT'S BEEN STUDIED FOR A LONG TIME BUT I THINK THERE'S AN INCREASING RECOGNITION THAT THERE ARE VERY SIGNIFICANT DISPARITIES IN TERMS OF CANCER INCIDENCE AND MORTALITY DETERMINED BY WHETHER THE COUNTY
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YOU LIVE IN IS RURAL VERSUS URBAN. RURAL POPULATIONS ARE MORE LIKELY TO HAVE INCREASED CANCER INCIDENCE, CONCERN CANCERS. IN TERMS OF MORTALITY HIGHER BURDEN. IT COULD BE UNEQUAL BURDEN OF POLLUTION, WE TOUCHED ON THAT EARLIER BUT SOCIO SOCIOECONOMIC STATUS IS LOWER IN CERTAIN RURAL AREAS AND IT GOES TO ACCESS TO HEALTH CARE, FINANCIAL ACCESS TO HEALTH CARE BUT ALSO GEOGRAPHICAL ACCESS TO HEALTH CARE BECOMES EXCEPTIONAL IMPORTANT. THIS IS JUST AGAIN SOME COLLECTIVE STUDIES SHOWING RURAL
1:14:13
CANCER DISPARIIES HAVE INCLUDED HIGHER RATES OF TOBACCO-ASSOCIATED CANCERS. THIS IS PRIMARILY BECAUSE THE PREVALENCE OF SMOKING IN RURAL AREAS IS HIGHER THAN IT IS IN URBAN AREAS. AGAIN, THAT GETS BACK TO YOU CAN SEE HOW IT'S INTERTWINED BECAUSE IN GENERAL THERE TENDS TO BE REDUCED ACCESS TO PREVENTIVE SERVICES. WHAT'S BEEN SEEN RECENTLY IN FACT IS WHILE TEMPORAL TRENDS HPV ASSOCIATED CANCER IS STABLE IN URBAN AREAS WE SEE INCREASE IN RURAL AREAS. AND THAT'S SOMETHING THAT NEEDS
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TO BE KEENLY MONITORED. THE REASON THESE THINGS NEED TO BE MONITORED IS BASED ON THIS. IT'S ALL ABOUT IMPACT. THAT IS ONCE WE START TO SEE TRENDS EMERGE, LIKE JUST USING THIS AS EXAMPLE, TOBACCO-ASSOCIATED CANCERS, WE KNOW THAT ACCESS TO TOBACCO CESSATION INTERVENTION IS A PROVEN METHOD AND IN TERMS OF HPV VACCINATION IF WE SEE INCREASING TREND FROM POLICY PERSPECTIVE THAT'S AN OPPORTUNITY TO INTRODUCE WAYS TO PREVENT THOSE CANCERS. THIS IS JUST SOME RECENT WORK BY THE CDC.
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TO TAKE YOU THROUGH THIS, THIS IS A PART OF A BIGGER PICTURE, THE REFERENCE AT THE BOTTOM SHOWS YOU ESSENTIALLY THE MORE BROWN THE COLOR, THE MORE URBAN THE COUNTY OR THE AREA WHERE THE PERSON LIVES. AGAIN, JUST IF YOU LOOK AT LUNG CANCER OVERALL THE INCIDENCE OF LUNG CANCER IS MUCH HIGHER IN RURAL AREAS. WE THINK THAT'S LARGELY BECAUSE OF THE HIGHER EXPOSURE TO TOBACCO. YOU SEE FOR BREAST CANCER YOU SEE HIGHER IN-- SORRY, HIGHER INCIDENCE OF BREAST CANCER IN THE MORE URBAN AREAS.
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AND I PUT UP THIS GRAPH TO MAKE THE POINT, I DON'T WANT TO LEAVE YOU WITH THE IMPRESSION EVERY CANCER IS HIGHER AND HAS HIGHER INCIDENCE AND MORTALITY IN RURAL COMPARED TO URBAN. THAT'S NOT THE CASE. IN GENERAL, YES, WE SEE THAT THERE'S A DISPARITY IN CANCER IN RURAL AREAS, BUT IT IS COMPLEX. SO FOR ANYONE WHO HAS AN INTEREST IN THE AREA, THIS IS ACTUALLY A GOOD PRIMER TO GET YOU INTERESTED IN IT. IT'S VERY RECENT DATA, SOME OF THE MOST RECENT DATA THEY HAVE. IN THE BOX HERE ON THE LEFT
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SHOWS INCIDENCE AND ON THE RIGHT SHOWS THE DEATH OR MORTALITY RATE. SO SOME STUDIES AS WELL WE HAVE DONE ACTUALLY ALSO IN COLLABORATION WITH CDC WAS AS I MENTIONED MY LAB IS INTERESTED IN LUNG CANCER, INTERESTED IN DISPARITIES. ONE OF THE QUESTIONS WE HAD IS SO WE KNOW IF YOU LOOK AT THE ENTIRE POPULATION THE INCIDENCE OF LUNG CANCER VARIES 30 TO 40% HIGHER IN AFRICAN-AMERICANS COMPARED TO EUROPEAN-AMERICANS. BUT THAT VERY FIRST PICTURE I SHOWED ABOUT GEOGRAPHY SHOWS VERY MIXED LANDSCAPE, RIGHT?
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DEPENDING ON WHERE YOU LIVE DISPARITIES COULD BE HIGHER OR LOWER. WE WANTED TO IN A GRANULAR WAY ASK THE QUESTION WHETHER OR NOT YOU WERE LIVING IN RURAL OR URBAN AREA BY COUNTY LEVEL, DETERMINE THE HOT SPOTS OF DISPARITY. WE LEARNED WHETHER IT'S FOR AN ADENOCARCINOMA OR SQUAMOUS CELL ARE TWO TYPES, THIS IS A LUNG CANCER STUDY, BUT NO MATTER WHAT TYPE WE STUDIED INCIDENCE WAS HIGHER IN AFRICAN-AMERICANS COMPARED TO EUROPEAN-AMERICANS. THE SECOND THING WE LEARNED IS THAT THE MORE RURAL YOUR
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LOCATION WAS IN TERMS OF WHERE YOU LIVE, THE HIGHER THE DISPARITY. NOW, THIS COULD BE DUE TO TOBACCO AND IN FACT WE HYPOTHESIZE IT'S BECAUSE OF TOBACCO, BUT THE ISSUE IS THAT -- TWO ISSUES. THE FIRST IS THE STUDY WITH THE CDC, THEY COLLECT DATA ON THE REGISTRIES, YOU DO NOT GET INDIVIDUAL DATA SO THE QUESTION CAN'T BE ASKED. I MENTIONED EARLIER THE INCIDENCE OF -- I'M SORRY, PREVALENCE OF SMOKING IS HIGHER IN RURAL AREAS. WE AS YET HAVE NO STUDIES I'M AWARE OF THAT THOSE PREVALENCE
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OF SMOKING IN RURAL AREAS IS HIGHER IN AFRICAN-AMERICAN VERSUS EUROPEAN-AMERICANS. IT SHOWS THESE TYPES OF STUDIES ALLOW US TO LOOK IN A GRANULAR WAY TO UNDERSTAND WHAT'S HAPPENING, IMPORTANT BECAUSE IF THERE ARE PREVENTIVE INTERVENTIONS SUCH AS SCREENING WE KNOW THE AREAS AND PEOPLE WE NEED TO TARGET IT TO. OKAY. I MENTIONED TOBACCO QUITE A BIT. I'M GOING TO TALK ABOUT IT A LITTLE BIT MORE. MOST OF WHAT I'M SEEING IN TERMS OF TOBACCO APPLIES TO LUNG CANCER BUT MANY OF YOU PROBABLY
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KNOW FROM ATTENDING THIS COURSE ALREADY THAT TOBACCO JUST ISN'T ASSOCIATED WITH LUNG CANCER. PANCREATIC BLADDER MANY DIFFERENT TIMES OF CANCER ARE ASSOCIATED WITH TOBACCO EXPOSURE. SO WHAT I'VE SHOWN HERE, I NOTICE THIS IS CUT OFF AT THE END A LITTLE BIT BUT BASICALLY THE INCIDENCE OF LUNG CANCER IN MANY, PARTICULARLY IN MEN, BUT IN THE UNITED STATES, IS HIGHEST AMONGST AFRICAN-AMERICANS. NOW, WE'VE TOLD YOU SMOKING IS THE CAUSE. WHEN YOU LOOK AT TOBACCO YOU EXPECT A SIMILAR CURVE BUT YOU DON'T.
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THE INCIDENCE OF HEAVY SMOKING, 15 CIGARETTES PER DAY OR MORE, YOU DON'T SEE THE SAME TREND AS UP HERE. EVEN THOUGH LUNG CANCER INCIDENCE IS HIGHER IN AFRICAN-AMERICANS THEY HAVE THE SECOND TO LOWEST PREVALENCE OF HEAVY SMOKING. YOU MIGHT SAY WHY IS THAT? YOU COULD GIVE AN ENTIRELY LECTURE HOW TO MEASURE SMOKING IN EPIDEMIOLOGIC STUDIES, NEIL MENTIONED THIS, I'LL GO THROUGH THE FACTORS. THERE IS A PARADOX BETWEEN WHAT WE KNOW ABOUT LUNG CANCER AND SMOKING, DISPARITIES, AND THE
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RELATIONSHIP BETWEEN -- TRIANGULAR RELATIONSHIP BETWEEN THE THREE VARIABLES. SO EVEN THOUGH THE PREVALENCE OF SMOKING IS LOWER OR ABOUT THE SAME IN AFRICAN-AMERICANS COMPARED WITH EUROPEAN-AMERICANS THE INCIDENCE OF LUNG CANCER IS HIGHER. WE KNOW THEY TEND TO START SMOKING LATER IN LIFE, CUMULATIVE EXPOSURE IS LOWER. ALSO REMEMBER I TOLD YOU THEY ARE DIAGNOSED EARLIER THAN EUROPEAN-AMERICANS. WHAT'S INTERESTING IS A STUDY SHOWED LOOKING AT NEVER SMOKERS, HAVING SMOKED 100 OR FEWER OVER
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THEIR LIFETIME. IN THAT STUDY YOU CAN SEE DISPARITIES. ONE OF THE BIGGEST DIFFERENCE IN TOBACCO EXPOSURE IS TYPE OF CIGARETTES USED IN THE UNITED STATES. VARIOUS REASONS, PRIMARILY MARKETING REASONS, ABOUT 760 TO 8 -- 70 TO 80% OF AFRICAN-AMERICANS USE MENTHOL. PEOPLE THOUGHT USE OF MENTHOL WAS ASSOCIATED -- OR CONTRIBUTED TO THE DISPARITIES. BUT IN FACT IT'S BEEN SHOWN THE INCIDENCE OF -- HIGHER INCIDENCE OF LUNG CANCER DOES NOT SEEM TO BE RELATED TO DISPARITIES --
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DOES NOT SEEM TO BE RELATED TO MENTHOL CIGARETTES. STUDIES HAVE ACTUALLY SHOWN IF YOU COMPARE MENTHOL TO NON-MENTHOL THE INCIDENCE IS HALF. IT DOESN'T SEEM AS THOUGH MENTHOL CIGARETTES COMPARE TO DISPARITIES, IF ANYTHING THEY CONFOUND IT MORE BECAUSE OF THE POINT I JUST MENTIONED. WE DON'T REALLY UNDERSTAND THAT. WHAT WE DO KNOW, HOWEVER, IS THAT AFRICAN-AMERICANS ARE LESS LIKELY TO QUIT SMOKING. AND A LOT OF STUDIES HAVE BEEN CONDUCTED TO -- AND SHOW THIS SEEMS TO BE PRIMARILY DUE TO --
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A LOT SEEMS TO BE DUE TO USE OF MENTHOL CIGARETTES. MENTHOL CIGARETTES ARE TRADITIONAL CIGARETTES BUT THEY HAVE THE COMPOUND MENTHOL ADDED TO THEM. WHAT THE MENTHOL DOES, CAUSES COOLING SENSATION IN THE BACK OF THE THROAT. A LOT OF IRRITANTS ONE MIGHT NORMALLY BE EXPOSED TO ARE IN A SENSE NULLIFIED. STUDIES HAVE SHOWN PEOPLE WHO SMOKE MENTHOL CIGARETTES ARE LESS LIKELY TO GIVE UP, THAT DO CONTRIBUTE TO DISPARITIES. IT'S IMPORTANT TO SHOW THIS IS A STUDY FROM CHRIS HINEMAN, A
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NUMBER OF YEARS AGO. IF YOU BREAK IT DOWN ACROSS RACIAL AND ETHNIC GROUPS AND GENDER, AFRICAN-AMERICANS ARE THE HIGHEST LEVEL FOR MEN AND WOMEN. AS YOU SMOKE MORE CIGARETTES MAGNITUDE OF DIFFERENCE IS ATTENUATED. THAT'S LIKELY AGAIN DUE TO THE INTENSE CARCINOGENICITY OF TOBACCO ITSELF. BEFORE I GO, THERE ARE SEVERAL THINGS THAT MANY ADDITIONAL THINGS YOU COULD SAY ABOUT THIS TOPIC. BUT ONE OF THE MOST IMPORTANT IS THAT EVEN FROM THE INITIAL STUDIES GOING BACK TO, YOU KNOW,
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ALL OF THOSE STUDIES THAT SHOW SMOKING WAS ASSOCIATED WITH LUNG CANCER, THERE IS A DIFFERENCE IN THE EFFECT OF -- MAGNITUDE OF EFFECT OF DURATION OF SMOKING VERSUS INTENSITY. YES, BOTH ARE ASSOCIATED WITH CANCER RISK BUT IN DIFFERENT -- THEY ARE NOT EQUAL IN A SENSE. SO WHAT MANY STUDIES HAVE NOW SHOWN IS THAT THE DURATION OF TOBACCO EXPOSURE IS MORE ASSOCIATED WITH LUNG CANCER RISK THAN THE ACTUAL INTENSITY. AND SO BECAUSE AFRICAN-AMERICANS ARE LESS LIKELY TO QUIT SMOKING,
1:24:14
ONE OF THE HYPOTHESES AT THE MOMENT IS THAT'S ONE OF THE FACTORS THAT'S DRIVING DISPARITIES. IN ADDITION TO TRYING MEASURE SMOKING IN EPIDEMIOLOGICALL STUDIES IT'S DIFFICULT, SOME STUDIES SHOWS SHOW IN LOW SOCIOECONOMIC STATUS ARE MORE LIKELY TO SMOKE MORE OF THE CIGARETTE THAN SOMEBODY WHO MIGHT HAVE UNLIMITED FINDS TO BUY 14 PACKS A DAY, IF THEY WANTED TO. SMOKING TENDS OF A SINGLE CIGARETTE IS MORE EFFICIENT IN THE POOR. IN AN EPIDEMIOLOGICAL STUDY IF I ASK HOW MANY YOU SMOKE, YOU SAY
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TEN, THE OTHER PERSON SAYS TEN, ONE PERSON MIGHT HAVE SMOKED EVERY BIT OF THE CIGARETTE, ANOTHER PERSON MAY HAVE SMOKED HALF. THE DOSE IN TERMS OF EPIDEMIOLOGICAL STUDIES IS NOT EQUIVALENT. NEIL TALKED ABOUT THIS, WHERE THINGS CAN GO WRONG IN TERMS OF MEASURING EXPOSURES. IN TERMS OF MEASURING TOBACCO AGAIN DEPENDING HOW DEEPLY SOMEBODY INHALES INTO THEIR LUNGS YOU CAN GET INCREASED EXPOSURE, WHETHER YOU SMOKE FIRST THING IN THE MORNING COMPARED TO THE CIGARETTES LATER
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ON IN THE DAY, ALL OF THESE THINGS MAKES MEASURING SMOKING EXTREMELY COMPLEX, SO SOME STUDIES WE'RE TRYING TO DO IN LUNG CANCER AND DISPARITIES IS TRY TO UNTANGLE SOME OF THAT COMPLEXITY AND AT LEAST MEASURE SMOKING IN A MORE GRANULAR WAY THAN WE HAVE BEEN DOING FROM THE STUDIES WITH THE IDEA THAT MIGHT GIVE US MORE INSIGHT INTO WHY WE'VE SEEN THE PARADOX BETWEEN SMOKING, LUNG CANCER AND DISPARITIES. MOST OF WHAT I'VE TALKED ABOUT HERE IS OF COURSE IS TERMS OF INCIDENCE.
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IT'S IMPORTANT TO REMEMBER SOMETHING NOT OFTEN APPRECIATED THE FACT THAT REGULAR SMOKING AFTER A CANCER DIAGNOSIS, NOT JUST FOR LUNGS, THIS IS FOR MANY DIFFERENT TYPES OF CANCER, SMOKING TOBACCO AFTER DIAGNOSIS IS ALSO ASSOCIATED WITH INCREASE LIKELIHOOD OF DEATH. OBVIOUSLY SIZE SHOWN FOR LUNGS BUT FOR MANY CANCER TYPES IT'S ALSO BEING SHOWN THAT SMOKING CONTRIBUTES TO MORTALITY. THE REASON THIS IS IMPORTANT, I MENTIONED EARLIER, AFRICAN-AMERICANS ARE LESS LIKELY TO QUIT TOBACCO USE.
1:26:24
FROM THE POLICY PERSPECTIVE AND INTERVENTION PERSPECTIVE, WHAT THIS SUGGESTS IS AT THE TIME OF CANCER DIAGNOSIS AGAIN NO MATTER YOUR CANCER TYPE, IF ANOTHER POINT OF INTERVENTION, WHERE NURSE PRACTITIONERS, DOCTORS, EVERYONE CAN HELP INTERVENE TO HELP THE PATIENT GIVE UP SMOKING, REGARDLESS OF RACE, TO SHOW IN TERMS OF DISPARITIES THIS IS ALSO A FACTOR THAT COULD BE CONTRIBUTING TO DIFFERENT MORTALITY OUTCOMES WE SEE. OKAY. I'LL JUST LEAVE IT THERE FOR NOW. IN TERMS OF MORTALITY, WE
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MENTIONED EARLIER ACROSS PRETTY MUCH MOST CANCER TYPES AFRICAN-AMERICANS HAVE THE HIGHEST MORTALITY RATES. ONE OF THE KEY DRIVERS IS THE STAGE AT WHICH CANCER IS DIAGNOSED. WE KNOW THIS IS THE FIGURE THAT'S PUBLISHED EVERY YEAR FROM THE AMERICAN CANCER SOCIETY AND IT'S UPDATED. WHAT IT BASICALLY SHOWS IS THAT FOR MOST CANCER TYPES, THERE IS A HIGHER LIKELIHOOD CANCER WILL BE DIAGNOSED AT LATER STAGE AMONG BLACKS AND AFRICAN-AMERICANS. AND THIS IS INCREDIBLY IMPORTANT BECAUSE THE LATER A TUMOR IS
1:27:45
DIAGNOSED, THE FEWER TREATMENT OPTIONS ARE AVAILABLE TO YOU. WE SEE THIS TREND YEAR AFTER YEAR. OKAY. SO WHY ARE TUMORS DIAGNOSED AT A LATER STAGE? WE GET INTO OUR FACTORS ON THE SLIDE SOCIETAL SOCIAL DETERMINANTS OF HEALTH, ACCESS TO CARE. ONE OF THE KEY QUESTIONS OF COURSE, THIS IS RELATED TO ACCESS TO CARE, DOES SCREENING MATTER. THE ANSWER IS YES, IT DOES. PERHAPS ONLY FOR SOME. LET ME EXPLAIN. WE DO KNOW THAT IF YOU LOOK AT -- STUDIES SHOW IF YOU LOOK AT MAMMOGRAPHY SCREENING IN AN
1:28:25
EQUAL ACCESS TO CARE SETTING THERE'S NO DIFFERENTIAL USE IN UPTAKE. THERE ARE SOME SITUATIONS WHERE THAT IS DIFFERENT. WE KNOW THAT AGAIN EVEN IN EQUAL ACCESS TO CARE SETTINGS, COLORECTAL SCREENING IS LOWER IN AFRICAN-AMERICANS IN REGIONS AROUND APPALACHIAN, YES, ACCESS TO SCREENING IS LOW BUT WHEN ACCESS IS LOW UPTAKE IS LOW. WE'LL TALK ABOUT UPTAKE IN A MOMENT. IT'S ALSO IMPORTANT TO MENTION THAT YES, SCREENING IS IMPORTANT, BUT EVEN IN CANCERS WHERE THERE'S NO VALIDATED
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SCREENING MOW MODALITY, IT'S IMPORTANT TO REMEMBER THAT. AS I MENTIONED, I WAS TALKING ABOUT LUNG CANCER. FOR MANY CANCER TYPES, LET ME JUST GO BACK. MANY CANCER TYPES IF THERE IS A SCREENING MODALITY AVAILABLE IT COULD BE ACCESS TO CARE THAT DETERMINES WHETHER OR NOT YOU'RE ABLE TO USE IT OR COULD BE YOUR OWN BELIEF SYSTEM THAT DETERMINES WHETHER OR NOT YOU USE IT. ANOTHER KEY CRITERION THAT DETERMINES WHETHER OR NOT HAVE YOU ACCESS TO SCREENING IS WHETHER OR NOT YOU FALL INTO THE
1:29:30
SCREENING GUIDELINES. SO FOR LUNG CANCER THE SCREENING GUIDELINES, THERE'S NOW A VALIDATED METHOD FOR LUNG CANCER SCREENING, LOW DOSE CT SCREENING REDUCES MORTALITY BY 20%, HIGHLY EFFECTIVE MODULE FOR REDUCING MORTALITY OF LUNG CANCER. OF COURSE FOR ANY SCREEN MODALITY THERE'S A SET OF CRITERIA. FOR LUNG CANCER, HEAVY SMOKER, MORE THAN 30 PACK YEARS OF SMOKING, AGE BETWEEN CURRENTLY 55 AND IT VARIES, 55 AND 74. I TOLD YOU TWO KEY THINGS, AGE OF DIAGNOSED IS EARLIER, AND
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SECONDLY I SHOWED YOU ON THE GRAPH THERE'S SIGNIFICANTLY LESS LIKELY TO BE HEAVY SMOKERS SO THERE'S A PORTION OF AFRICAN-AMERICANS YOU'RE GOING TO INCLUDE IN SCREENING CRITERIA IS LOWER, THIS IS A STUDY WE DID USING OUR CASE CONTROL STUDY THAT HIGHLIGHTS THAT. SO HERE IS THE UNITED STATES PREVENTIVE SERVICES TASK FORCE RECOMMENDATION SERVICES FOR LUNG CANCER SCREENING, THIS IS THE CRITERIA CMS APPROVE. IF YOU USE THOSE CRITERIA AFRICAN-AMERICANS ARE LESS LIKELY TO BE INCLUDED IN THE
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SCREENING CRITERIA. THIS IS SHOWN FOR COLORECTAL CANCER, I THINK BREAST AND PROSTATE AS WELL, IT'S LED TO A DISCUSSION ABOUT WHETHER IT'S IMPORTANT TO HAVE POPULATION-SPECIFIC SCREENING CRITERIA OR INTRODUCE OTHER METRICS THAT MIGHT BE IMPORTANT, YOU KNOW, OTHER RISK FACTORS, FAMILY HISTORY, COPD, A FEW THINGS IN LUNG, IN FACT THERE'S A STUDY DONE BY COLLEAGUES IN DCEG IF YOU INCLUDE MORE RISK FACTORS NOT JUST SMOKING EXPOSURE, WHAT YOU CAN DO IS YOU WILL END UP INCREASING INCLUSION
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OF MORE HIGH RISK GROUPS AND THAT'S WHY IT'S IMPORTANT. STUDIES ARE NOW BEING CONDUCTED INCLUDING SOME IN OUR LABORATORY TO TRY AND FOLLOW THESE SPECIFIC SCREENED DETECTED CANCERS OVER TIME BECAUSE IF YOU HAVE A CONCERN POPULATION AT HIGH RISK FOR LUNG CANCER SUCH AS AFRICAN-AMERICANS, THEY ARE PROPORTIONATELY EXCLUDED FROM SCREENING, JUST BY INTRODUCING SCREENING AS A GOOD THING THERE COULD BE UNINTENDED CONSEQUENCE YOU COULD LEAD TO INCREASE IN DISPARITIES, THESE ARE THINGS
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WE'RE AWARE OF AND NEED TO FOLLOW ON AN ANNUAL BASIS SO IF THESE DISPARITIES DO TEND TO -- IF THEY TEND TO WIDEN WE CAN HOPEFULLY INTERVENE IN A TIMELY FASHION. OKAY. I MENTIONED THIS EARLIER, ACCESS TO CARE IS VERY IMPORTANT. ONE OF THE DEDETERMINANTS IS INSURANCE STATUS. THIS GRAPH SHOWS FOR MANY CANCERS, THERE'S OTHERS IN THIS PAPER, BUT WHAT IT SHOWS IS THAT DEPENDING ON WHETHER YOU'RE INSURED, HAVE ACCESS TO MEDICARE OR HAVE NO INSURANCE, THE GREEN LINE SHOWS PEOPLE THAT HAVE INSURANCE.
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FOR EVERY CANCER TYPE, EVEN THOSE WITH DISMAL SURVIVAL SUMP AS LUNG CANCER OUTCOME IS BETTER AMONG THOSE THAT HAVE INSURANCE. IN TERMS OF DISPARITIES IN CANCER MORTALITY ONE OF THE KEY METRICS I WANT YOU TO TAKE AWAY IS ACCESS TO CARE DEFINITELY MATTERS. THIS SLIDE BRINGS IT HOME, JUST LOOKING AT LUNG CANCER, SURVIVAL DISPARITIES BETWEEN AFRICAN-AMERICANS AND EUROPEAN-AMERICANS, EQUAL ACCESS TO CARE SITTING. THIS WAS DONE ACROSS THE STREET AT WALTER REED MEDICAL CENTER.
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IT SHOWS IN THIS CONTEXT IF EVERYBODY HAS SAME ACCESS TO CARE THERE'S NO DIFFERENCE IN SURVIVAL. IT'S A VERY CLEAR I THINK AND UNEQUIVOCAL MESSAGE. I ALSO DON'T WANT YOU TO LEAVE YOU WITH THE INTENT -- WITH THE IMPRESSION THAT FOR EVERY CANCER TYPE, AFRICAN-AMERICANS ALWAYS DO WORSE. THAT'S NOT NECESSARILY THE CASE. THIS IS JUST ONE EXAMPLE HERE FOR MULTIPLE MYELOMA. THIS IS AN INTERESTING CANCER BECAUSE AFRICAN-AMERICANS ARE CERTAINLY MORE LIKELY TO DEVELOP THE PRECURSOR MGUT, WHERE YOU'RE
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ALREADY DIAGNOSED AFRICAN-AMERICANS TEND TO DO BETTER, I WANT YOU TO ALSO BE AWARE OF THAT. OKAY. TALKING MORE ABOUT ACCESS TO CARE, THIS IS A GRAPHIC GOING BACK TO THE ENTIRE UNITED STATES, WHAT IT SHOWS IS WHAT'S GRAPHED IS THE ONCOLOGISTS, NUMBER OF ONCOLOGISTS PER 100,000 RESIDENTS. AGAIN LIGHTER COLORS REPRESENT ZERO, WHICH IS NONE, ACCESS TO NO ONCOLOGIST VERSUS ACCESS TO MORE THAN EIGHT. IT VARIES QUITE DRAMATICALLY ACROSS THE U.S. AGAIN, YOU CAN EVEN THINK IN
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YOUR MIND, YOU CAN SEE HOW THAT COULD INFLUENCE BOTH YOUR ACCESS TO CARE, BUT ALSO YOUR OUTCOMES. ACCESS TO CARE, IT'S IMPORTANT. IT'S NOT JUST ACCESS TO CARE BUT UTILITY AND UPTAKE OF THAT CARE. AGAIN FOCUSING ON LUNG CANCER THIS HAS BEEN SHOWN IN 90 STUDIES, I'LL COVER ONE OR TWO OTHERS, IN THIS REPORT IN 2010 THEY WENT THROUGH -- THIS IS WORK BY CHRIS LANDTHUM AND COLLEAGUES IN THIS AREA. EVEN IN A SETTING WHERE SOMEWHAT EQUAL ACCESS TO CARE, FOR SOME CASES AFRICAN-AMERICANS ARE LESS
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LIKELY TO RECEIVE SURGERY AND LESS LIKELY TO SEVERE CHEMOTHERAPY, SEEN CONSISTENTLY IN MANY STUDIES. COLORECTAL CANCER, EQUAL ACCESS TO CARE BUT AFRICAN-AMERICANS WITH COLON CANCER WERE LESS LIKELY TO RECEIVE SURGERY AND CHEMOTHERAPY. WE SEE THIS MANY IN MANY CANCER TYPES. YOU MIGHT ASK WHY IS THIS THE CASE? ONE OF THE CONTRIBUTING FACTORS, THIS IS WHERE THE BEHAVIORAL SCIENTISTS COME IN, THIS IS EXAMPLE FROM LUNG CANCER, IT SHOWS THAT PERCEPTION AND BEHAVIORS ARE IMPORTANT AND MATTER.
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IN TERMS OF LUNG CANCER THIS IS DATA FROM THE NATIONAL INFORMATION HEALTH SURVEY, TREND SURVEY, AND THEY FOUND THAT AGAIN JUST GOING BACK TO BELIEF AND SYMPTOMS, A LOT OF PEOPLE EXPECTED THERE TO BE SYMPTOMS ASSOCIATED WITH LUNG CANCER BEFORE YOU WOULD ACTUALLY HAVE A DIAGNOSIS. WE KNOW THAT'S NOT THE CASE. OFTEN TIMES SYMPTOMS FOR LUNG CANCER WHEN THEY APPEAR IT'S OFTEN STAGE 3 OR STAGE 4. AND AGAIN THIS SORT OF THING HAS BEEN SEEN IN MANY STUDIES AND FOR MANY CANCER TYPES.
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THE PERSONAL BELIEF SYSTEM TO STUDY AND UNDERSTAND ARE VERY COMPLEX BUT WE KNOW THEY PLAY AN IMPORTANT ROLE. IN ADDITION, THERE'S A LOT OF WORK THAT PETER HAS DONE IN NEW YORK TO STUDY THE PATIENT AND PHYSICIAN RELATIONSHIP AND HOW -- I DON'T KNOW IF YOU HAVE HAVE LECTURES ON UNCONSCIOUS BIAS IN THIS SERIES, I DON'T THINK SO, BUT AGAIN HOW DIFFERENT PATIENTS BUT ALSO PROVIDERS CAN JUST THROUGH AN UNCONSCIOUS MECHANISM BIAS RECOMMENDATION TO PATIENTS. A LOT OF BEHAVIORAL SCIENTISTS
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ARE STUDYING THOSE TYPES OF RELATIONSHIPS. THERE'S THE ISSUE OF COMORBID CONDITIONS. I MENTIONED CERTAIN POPULATIONS WERE LESS LIKELY TO UNDERGO SURGERY OR RECEIVE CHEMOTHERAPY BUT A LOT IS RELATED TO COMORBIDITIES. WHAT MAKES YOU A GOOD CANDIDATE FOR SURGERY MIGHT ACTUALLY IN ANOTHER PATIENT FOR EXAMPLE BMI, YOUR WEIGHT, IF YOU HAVE LUNG CANCER EMPHYSEMA COPD IT VARIES ACROSS POPULATION AND THAT CAN CONTRIBUTE TO THE REASONS WHY SOME PATIENTS MIGHT BE MORE LIKELY TO UNDERGO
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CHEMOTHERAPY OR SURGERY. THE OTHER POINT TO MENTION, WE'VE TALKED ABOUT ACCESS TO CARE, IT'S IMPORTANT. WE'VE TALKED ABOUT THE ACCESS AND UPTAKE OF CARE. BUT THE THIRD RUNG OF THIS VERY IMPORTANT LATTER IS ACCESS TO CARE DOES NOT MEAN EQUAL ACCESS TO GOOD CARE. AND SO WHAT DO I MEAN BY THAT? AGAIN IT GETS BACK A LITTLE BIT MAYBE TO THE GRAPH I SHOWED YOU OF THE UNITED STATES WHERE YOU HAD ACCESS TO ONCOLOGISTS. DOES THIS MEAN JUST BECAUSE YOU HAVE TWO AREAS THAT ARE YOU
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THERE BLUE THAT THEY ARE WELL TRAINED, ALL WENT TO HOPKINS AND IN ALL AREAS ARE OUTSTANDING PHYSICIANS, THAT'S NOT ALWAYS THE CASE. WHAT STUDIES ARE TRYING TO DELVE INTO MORE AND UNDERSTAND IN HOW TO UNDERSTAND DISPARITIES IS HOW ACCESS TO CARE DOES NOT ALWAYS MEAN ACCESS TO GOOD QUALITY CARE. A LOT OF THE PUBLIC HEALTH AND INTERVENTIONIST METHODS ONGOING RIGHT NOW ARE TRYING TO DEAL WITH THAT SPECIFIC TOPIC. AND TRY TO UNDERSTAND THIS AND APPRECIATE IT, ESPECIALLY WITH
1:38:43
ALL THE CONVERSATIONS THAT THERE ARE ABOUT THE AFFORDABLE CARE ACT AND HOW IT'S GOING TO IMPACT ACCESS TO CARE. IT'S IMPORTANT NOT TO LOSE SIGHT OF THE FACT THAT WHAT WE'RE TRYING TO DO IS INCREASE ACCESS TO GOOD QUALITY AND EQUAL QUALITY HEALTH CARE, THAT'S OFTEN AN UNMENTIONED PART BUT VERY IMPORTANT ONE. I'VE TALKED ABOUT MANY OF THE DIFFERENT PARTS OF MORE SOCIETAL FACTORS THAT CAN CONTRIBUTE TO CANCER HEALTH DISPARITIES. BUT I ALSO WANT TO TALK ABOUT A LITTLE BIT IN THE LAST 15
1:39:13
MINUTES OR SO HOW BIOLOGY IS ALSO IMPORTANT. SOME CANCERS EVEN IN AN EQUAL ACCESS TO CARE SETTING, EVEN WHEN YOU CONTROL FOR ALL THE FACTORS WE TALKED ABOUT THERE ARE DIFFERENCES IN SURVIVAL. THIS IS AN EXAMPLE, ONE GRAPH, BREAST CANCER, IT'S SHOWING AFRICAN-AMERICANS DO WORSE THAN EUROPEAN-AMERICANS. SO, AS I MENTIONED, IT'S NOT JUST BREAST CANCER. THERE'S OTHER CANCERS, THIS IS A CLINICAL TRIAL SETTING. WHAT THEY HAVE DONE IS COMPARED THE OUTCOMES BETWEEN EUROPEAN-AMERICANS AND
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AFRICAN-AMERICANS ACROSS SEVERAL CANCER TYPES. BASICALLY AGAIN ANY NUMBER ABOVE 1, THAT'S RED, MEANS SIGNIFICANT. IF IT'S ABOVE 1 IT MEANS AFRICAN-AMERICANS ARE MORE LIKELY TO DO WORSE. YOU CAN SEE HERE BREAST CANCER BOTH PRE AND POST MENOPAUSAL AND YOU CAN SEE OTHER CANCERS SUCH AS PROSTATE AND OVARIAN CANCER WHERE WE SEE THE SAME THING. SO IT STARTS TO FEEL IT'S COINCIDING WITH EXPLOSION EVER TECHNOLOGY, ASKING WHETHER OR NOT BIOLOGY OF CANCER IS DIFFERENT ACROSS DIFFERENT POPULATIONS.
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SO WE THINK ABOUT BIOLOGY, WHAT DO WE REALLY MEAN? WE'RE THINKING ABOUT GENE EXPRESSION PROFILES, METHYLATION, WE'RE THINK ABOUT SOMATIC MUTATIONS, GERM LINES, ETHICS, SYSTEMS BIOLOGY, ALL THE THINGS TO PROBE A TUMOR, WE TALK ABOUT BIOLOGY, THAT'S WHAT WE THINK ABOUT. A FEW EXAMPLES TO HIGHLIGHT FROM SOME LITERATURE IN THE AREA, FOR THOSE FAMILIAR WITH PROSTATE CANCER YOU MIGHT KNOW ITS AGGRESSIVENESS IS MEASURED IN THE GLEASON SCORE. ON THE LEFT YOU CAN SEE THE GLEASON SCORE OF 1 GENERALLY
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MOSTLY NORMAL CELLS, WHEREAS 5 IT'S COMPLETELY ABNORMAL. VARIOUS SCORES PUT THIS TOGETHER, AS A LINEAR SCALE. THE HIGHER IT IS, THE MORE AGGRESSIVE YOUR TUMOR IS. WHAT'S BEEN FOUND CONSISTENTLY ACROSS MANY DIFFERENT STUDIES INCLUDING WORK DONE BY STEPHAN, A TENURED INVESTIGATOR IN OUR LABORATORY IN CCR, WHAT THEY FOUND IS AFRICAN-AMERICANS TEND TO BE -- ONCE THEY ARE DIAGNOSED WITH PROSTATE CANCER, IT TENDS TO BE MORE AGGRESSIVE DISEASE, THAT'S BEEN FOUND IN MANY STUDIES.
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ONE THE OTHER INTERESTING THINGS, NEIL TOUCHED ON THIS WHEN HE TALKED ABOUT THE GENOME WIDE ASSOCIATION STUDIES, ALL THE STUDIES THAT HAVE BEEN DONE TO TRY AND UNDERSTAND FROM THE GERMLINE GENETICS PERSPECTIVE WHAT FACTORS CONTRIBUTE TO THE INCREASED INCIDENCE. WE'VE KNOWN FOR QUITE A WHILE NOW, THE GWAS STUDIES CONFIRM THIS, REGION OF 8Q24 IS ASSOCIATED WITH INCREASED RISK OF MANY CANCER TYPES, SPECIFICALLY PROSTATE CANCER. SEVERAL STUDIES FOUND NOW BY CHRIS SIMON AND FRIEDMAN AND
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OTHER COLLEAGUES IS THAT THE REGION, SPECIFIC REGION 8Q24 PARTICULARLY ASSOCIATED WITH PROSTATE CANCER, THAT REGION IS ENRICHED IN AFRICAN-AMERICANS. THEY HAVE BEEN ABLE TO ESTIMATE 50% OF THE INCREASED INCIDENCE SEEN AMONGST AFRICAN-AMERICANS WITH PROSTATE CANCER IS DUE TO THIS REGION. THERE DOES SEEM TO BE AT LEAST A GENETIC REASON OR GERMLINE REASON WHY PARTIALLY THERE'S AN INCREASED INCIDENCE OF PROSTATE CANCER IN THAT POPULATION. THERE'S ANY OTHER REGION 17Q21 THAT SEEMS TO BE CONTRIBUTED.
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COLLEAGUES IN DETROIT, WHAT THEY HAVE SHOWN IS THAT THIS REGION, THIS 8Q24 REGION SEEMS TO BE ASSOCIATED WITH THAT GLEASON SCORE I MENTIONED A MOMENT AGO. NOT ONLY IS IT MORE LIKELY TO GIVE RISE TO INCREASED INCIDENCE BUT TO THE MORE AGGRESSIVE FORM, LETHAL FORM. I MENTIONED TALKING ABOUT GERMLINE GENETICS. THIS GETS BACK TO -- THIS SLIDE TAKES YOU BACK TO WHAT WE TALKED ABOUT AT THE BEGINNING. WE TALKED ABOUT RACE. WE TALKED ABOUT ANCESTRY. RACE AND ANCESTRY AND ETHNICITY.
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RACE IN GENERAL TALKS ABOUT -- OR PERTAINS TO GENETIC ANCESTRY IN PART, WHERE ONE COMES FROM. WHAT WE KNOW IS THAT AFRICAN-AMERICAN POPULATIONS IN THE UNITED STATES ARE MIXED POPULATION. WE'RE THINKING ABOUT HOW AND WHETHER GENETICS CONTRIBUTE TO CANCER HEALTH DISPARITIES, WE ALSO NEED TO VERY CLEARLY CONSIDER WHETHER OR NOT THERE'S A LIKELIHOOD THAT THE POPULATION THAT WE'RE LOOKING AT ARE ETHNIC, SO FOR EXAMPLE I JUST TALKED ABOUT 8Q24 BEING MORE THAN FROM THE GERMLINE PERSPECTIVE.
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IF YOU LOOK AT HOMOGENOUS IT'S IMPORTANT TO CONSIDER. IF YOU LOOK AT A POPULATION WHERE DEGREE OF AFRICAN-AMERICAN ANCESTRY VARIES ALSO SOMETHING YOU NEED TO CONSIDER IN YOUR STUDIES. WHAT I'VE GRAPHED THEIRS ARE PARTICIPANTS IN OUR CASE CONTROL STUDY, 1500, WHAT'S SHOWN IN GREEN IS THE DEGREE EVER WEST AFRICAN ANCESTRY, IN BLUE NATIVE AMERICAN ANCESTRY, AND IN THE YELLOW COLOR IS DEGREE OF EUROPEAN ANCESTRY. ALL OF THE PEOPLE ON THIS GRAPH HAVE SELF REPORTED BEING AFRICAN-AMERICAN.
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WHAT YOU SEE IS THAT THE DEGREE OF EUROPEAN ANCESTRY IN THESE PEOPLE VARIES QUITE A BIT. YES CERTAINLY DOWN HERE ONE OR TWO OF THE PEOPLE COULD HAVE BEEN AN AREA -- CLEARLY THE PERSON IS 95% EUROPEAN ANCESTRY, YES THAT COULD BE A MISTAKE IN TERMS OF HOW THE DATA WERE RECORDED OR SOMETHING LIKE THAT BUT REGARDLESS WHAT THE POINT SHOWS IS THAT ACROSS A A SINGLE POPULATION WHAT IT SHOWS IS FROM A GENETIC PERSPECTIVE LOOKING FOR THINGS BIOLOGICALLY AND GENETICALLY CONTRIBUTING TO
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DISPARITIES WE NEED TO BE AWARE OF UNDERLYING ANCESTRY IN POPULATION AND ACCORDINGLY ADJUST FOR IT. THERE'S THE SELF REPORT OF YOUR ANCESTRY AND ETHNICITY WHICH CAN OFTEN PERTAIN TO YOUR BEHAVIOR AND LIFE STILL AND EXPOSURE AND DETERMINANTS ON YOUR HEALTH BUT ALSO TALKING ABOUT ANCESTRY AND GENETICS WE NEED TO CONSIDER THINGS LIKE THIS. OKAY. AND ACTUALLY INTERESTING IN OUR STUDY WHAT WE DID FIND IS THAT INCREASING WEST AFRICAN ANCESTRY IS ASSOCIATED WITH LUNG CANCER
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RISK AND WE SEE THIS ONLY IN MEN, NOT WOMEN. OKAY. ON THE GRAPH I MENTIONED EARLIER ONE OF THE THINGS WE ALSO MEASURED IN TERMS OF EUROPEAN ANCESTRY AND AFRICAN ANCESTRY WAS NATIVE AMERICAN ANCESTRY. A VERY INTERESTING STUDY PUBLISHED A COUPLE YEARS AGO HAS SHOWN INCREASING PROPORTION OF NATIVE AMERICAN IS ASSOCIATED WITH ACUTE CHILDHOOD LYMPHOBLASTIC LEUKEMIA. SEEMS TO BE SOMEWHAT SPECIFIC. WHAT'S ALSO INTERESTING AND GIVES IDEA HOW THIS IMPORTANT FROM INTERVENTION PERSPECTIVE
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ALSO SHOWING IT'S RELATED TO& THERAPEUTIC OUTCOMES. IN A STUDY THEY FOUND CHILDREN WHO HAD MORE THAN 10% NATIVE AMERICAN ANCESTRY NEEDED AN ADDITIONAL ROUND OF CHEMOTHERAPY TO RESPOND TO THE DRUG. THEY ARE NOW ABLE TO STRATIFY PATIENTS IN THIS CASE PATIENTS WITH CHILDHOOD ACCUSE LYMPHOCYTIC LEUKEMIA AND TARGET FOR EXTRA ROUND OF CHEMOTHERAPY TO SEE THE SAME RESPONSE. IT SHOWS THAT ANCESTRY IN TERMS OF DISPARITY STUDIES OR JUST CLINICAL MEDICINE IS IMPORTANT AND IS RELEVANT.
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WE'VE TALKED ABOUT GERMLINE GENETIC. SOMATIC GENETICS ARE ALSO OF INTEREST AND IMPORTANCE, SOMETHING WE STUDY IN OUR LAB. I'M GOING TO GIVE YOU AN EXAMPLE OF A STUDY IN COLORECTAL CANCER. OBVIOUSLY, LUNG CANCER IS ONE OF THE SIMILAR EXAM PELTS. -- EXAMPLES. WE'RE NOT LOOKING FOR EVERYTHING WILL NOT BE DIFFERENT. IN THE CASE OF LUNG CANCER, SMOKING CAUSES LUNG CANCER, MOST OF THE POPULATIONS THAT DEVELOP LUNG CANCER HAVE SMOKED. A LOT OF GENE EXPRESSION CHANGES WILL BE THE SAME BUT THE FOCUS
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OF SOME STUDIES IS TRYING TO UNDERSTAND WHAT IS SIMILAR AND WHAT IS DIFFERENT. SO IN THIS SITUATION HERE WHAT THEY FOUND IS THAT MUTATIONS SPECIFICALLY IN EPHA6 AND FLCN, 3%, 4%, 5%, MAYBE 6%, NOT ALL MUTATIONS FOUND IN POPULATIONS OF EUROPEAN ANCESTRY. YOU MIGHT ASK YOURSELF SO WHAT? MAYBE SOME OF THESE MUTATIONS ARE ACTIONABLE. MAYBE SOME MUTATIONS COULD BE TARGETS FOR CANCER VACCINES. A LOT OF WORK IS GOING ON NOW WITH PIC3A, FOR EXAMPLE, A LOT OF RESEARCH GROUPS ARE TRYING TO
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FIGURE OUT CAN WE DEVELOP CANCER VACCINES FOR THOSE EPITOPES. IF THE MUTATIONS ARE NOT PRESENT IN ONE POPULATION THE VACCINES WILL NEVER WORK. THAT'S WHY LOOKING AT RACIAL DIFFERENCES IN TERMS OF SOMATIC GENETICS IS ALSO VERY IMPORTANT. AND THIS IS AGAIN GOING BACK TO PROSTATE CANCER TO SHOW YOU YOU MIGHT HAVE HEARD OF THE TMPRSS2: ERG, THERE ARE GEOGRAPHIC AND RACIAL DIFFERENCES IN THE PRESENCE OF ONCOGENE, P10 AND OTHER PREVALENT MUTATIONS BUT THE FINDING FOR ERG HAS BEEN
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FOUND, HAS BEEN KNOWN FOR QUITE A WHILE. IT'S NOT JUST IN TERMS OF EUROPEAN-AMERICANS AND AFRICAN-AMERICAN AMERICANS. THE FREQUENCY OF THIS MUTATION IS DIFFERENT IN ASIAN POPULATIONS AND AGAIN IN LUNGS WE KNOW EGFR MUTATIONS ARE MORE PREVALENT IN POPULATIONS OF ASIAN DESCENT, SOME REPORTS IT'S DIFFERENT IN AFRICAN-AMERICANS AND EUROPEAN-AMERICANS HERE IN THE UNITED STATES, BUT IT'S NOT AS DIFFERENT AS ASIAN POPULATIONS. SO BY LOOKING, THAT'S AGAIN ONE REASON THAT'S IMPORTANT, EGFR IS
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AN ACTIONABLE MUTATION SO PATIENTS THAT RECEIVE THAT THERAPY GENERALLY HAVE A BETTER OUTCOME. SO IT'S IMPORTANT NOT JUST TO STUDY AND TRY TO IDENTIFY NEW MUTATIONS BUT ALSO TO UNDERSTAND HOW THE PREVALENCE OF THEM DIFFERS ACROSS POPULATIONS. GETTING THEN A LITTLE BIT HIGHER UP IN THE ORDER, SO AGAIN SOME OF YOU MIGHT KNOW THIS, IT'S NOT JUST GERMLINE OR SOMATIC GENETICS THAT ARE DIFFERENT. IN THE ERA OF TECHNOLOGICAL DEVELOPMENT, THAT THE MOLECULAR SUBTYPES OF BREAST CANCER ARE
1:50:32
DIFFERENT ACROSS POPULATIONS. SO MANY OF YOU WILL HAVE HEARD OF LUMINAL A AND LUMINAL B, BUT THE BASAL TYPE OF CANCER, MORE LIKELY TORE ER, HER-2 NEGATIVE AND PR-NEGATIVE IS MORE PREVALENT IN AFRICAN THAN EUROPEAN DESCENT. THIS IS THE BASAL-LIKE SUBTYPE HERE. IT'S VERY PREVALENT, ESPECIALLY IN PRE-MENOPAUSAL AFRICAN-AMERICAN WOMEN BUT AT LEAST HALF IF NOT LESS PREVALENT IN OTHER POPULATIONS. THIS IS JUST ONE STUDY BUT IT'S BEEN FOUND AGAIN AND AGAIN. IF THESE TYPES OF STUDIES IT'S
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AN OBSERVATION. YOU ASK YOURSELF IS IT GENETIC, IS IT EXPOSURE? OBVIOUSLY WHY DIFFERENT IS IMPORTANT BUT AGAIN FOR BREAST CANCER THE FACT THAT IT IS DIFFERENT IS ALSO INCREDIBLY IMPORTANT. AGAIN, THE REASON IS AS I'M SURE YOU'VE COVERED ALREADY IN THE COURSE TRIPLE-NEGATIVE TYPE OF BREAST CANCER IS LESS AMENABLE TO THERAPEUTIC OPTIONS OUT THERE AT THE MOMENT. THAT'S ONE OF THE REASONS WHY IN TERMS OF DISPARITIES WHY BIOLOGY MATTERS. THIS IS A STUDY FROM A COUPLE YEARS AGO, BUT EVEN THOUGH THE
1:51:59
SUBTYPE IS MORE PREVALENT IN AFRICAN-AMERICANS, AND IT IS A PARTICULARLY POOR AND AGGRESSIVE SUBTYPE, THIS STUDY SHOWS US WHEN THEY LOOK AT THE MORTALITY OUTCOMES ACROSS VARIOUS SUBTYPES OF BREAST CANCER, NOT JUST TRIPLE-NEGATIVE, THERE'S STILL A DISPARITY. YES TRIPLE NEGATIVE IS A AN IMPORTANT PART OF DISPARITIES BETWEEN EUROPEAN-AMERICANS AND AFRICAN-AMERICANS, AFRICAN-AMERICAN WOMEN REGARDLESS OF SUBTYPE HAVE A WORSE OUTCOME, AN IMPORTANT MESSAGE I WANT YOU TO TAKE AWAY.
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THIS IS AN EXAMPLE OF WORK WE'VE DONE IN LUNG CANCER. WHEN WE LOOK AT GENE EXPRESSION PATHWAYS, IN LUNG CANCER WE DON'T HAVE THE SAME BREAKDOWN OF MOLECULAR SUBTYPES AS BREAST CANCER. THIS IS SIMILAR TO BREAST, COLON, A LOT OF PATHWAYS IN AFRICAN-AMERICAN ALSO ARE STEM CELL RELATED, AND MIGRATION RELATED, INVASION RELATED. WE'VE SEEN THAT IN OTHER CANCER TYPES. THE POINT IS THAT A LOT OF GENE EXPRESSION CHANGES THAT WE SEE IN LUNG CANCER ARE SIMILAR IN EUROPEAN AMERICANS AND
1:53:18
AFRICAN-AMERICANS, AND WE EXPECT THAT TO BE THE CASE BECAUSE AGAIN AS I SAID SMOKING CAUSES LUNG CANCER, WHAT WE'RE TRYING TO DO IS UNDERSTAND WHAT'S DIFFERENT AND CAN WE LEVERAGE AND TARGET IT. WITH THE NEWER TECHNOLOGIES THIS IS DATA THAT WAS BASED ON EXPRESSION RATES BUT NOW WE HAVE RNA-SEQ. WE HAVE TOOLS TO LOOK AT VARIANTS, SMALL RNA-SEQ, WE'RE USING ALL OF THESE TECHNIQUES RIGHT NOW TO GET A MUCH MORE GRANULAR VIEW OF BIOLOGY, THIS IS LIKE A HIGH LEVEL VIEW BUT
1:53:54
WE WANT TO UNDERSTAND EXACTLY WHAT THE DIFFERENCES ARE. WE'RE DOING IT IN LUNG, OTHERS ARE DOING ENDOMETRIAL, SOME BREAST AND PROSTATE. THERE ARE MANY INVESTIGATIONS ACROSS THE U.S. LOOKING INTO THIS AREA. I MENTIONED STEPH, THIS IS SOME WORK HE HAD DONE IN PROSTATE CANCER. YES, THERE ARE MANY SIMILARITIES BUT WHERE THERE ARE DIFFERENCES THE KEY DIFFERENCE IS THAT MANY OF THE PATHWAYS RELATE TO INFLAMMATION. SO I MENTIONED ONE OF THE REASONS WE STUDY BIOLOGY IS BECAUSE WE WANT TO UNDERSTAND
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FROM A TARGETING PERSPECTIVE IN TERMS OF THERAPY IF THERE'S A MUTATION CAN WE TARGET IT, IF THERE'S A SPECIFIC PATH PAY SPECIFIC TO ONCOGENES CAN WE TARGET IT. TO A STEP EARLIER, A LOT OF WORK WE DO IN TERMS OF BIOMARKERS IS BASED IN TUMOR BIOLOGY. WE TRY AND DETECT THE TUMOR EARLY, BEFORE YOU EVEN HAVE A DIAGNOSIS, TO PREDICT RISK, AND IN TERMS OF PROGNOSIS. IF THE BIOLOGY OF A TUMOR IS DIFFERENT, IT FOLLOWS IN SOME CASES THAT THE BIOMARKERS THAT WE USE TO DETECT THE TUMOR WILL
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ALSO BE DIFFERENT BECAUSE MOST OF THE BIOMARKERS WE STUDY ARE COMING FROM THE TUMOR ITSELF. AGAIN, FROM THE STUDIES IN OUR LABORATORY, IN ADDITION TO STUDYING THE TUMOR -- I'M SORRY, BIOLOGY OF THE TUMOR, IT'S FROM LOOKING AT BIOMARKERS, WE ASK THE QUESTION IN TERMS OF DISPARITIES. AGAIN WE SEE THINGS SIMILAR IN TERMS OF LUNG CANCER INFLAMMATION MARKERS, IL-6, IL-8 THERAPY, WE SEE THAT IN BOTH POPULATIONS. WE ALSO SEE DIFFERENCES AND FOR EXAMPLE THIS IS JUST TWO EXAMPLES, IL-1 BETA IS ONLY
1:55:37
ASSOCIATED WITH RISK IN AFRICAN-AMERICANS, THE SAME WITH IL-10. WE DON'T SEE IT IN EUROPEANS AMERICANS SUGGESTING AS WE MOVE FORWARD, TO TRY AND DEVELOP BIOMARKERS FOR THE EARLY DIAGNOSIS OF CANCER, AGAIN WE NEED TO THINK OF THE POPULATION-SPECIFIC WAYS SO WE HAVE THE HIGHEST ACCURACY FOR EACH POPULATION. HOPEFULLY AS WE'VE GONE THROUGH THE TALK I HAVE IN A HIGH LEVEL WAY POINTED OUT THERE ARE MANY DIFFERENT FACTORS THAT CONTRIBUTE TO DISPARITIES. WE WORK ON ONE SPECIFIC AREA,
1:56:14
FOCUSED ON BIOLOGY, BUT TO TRY AND UNDERSTAND THIS AND THEN IN ORDER TO ADDRESS IT THERE'S MANY DIFFERENT FACTORS INVOLVED AND SIMILARLY MANY DIFFERENT DISCIPLINES THAT ARE NEEDED TO TRY AND ADDRESS IT. IT'S EXTREMELY IMPORTANT TO EMPHASIZE THAT BECAUSE EVEN FROM A BIOLOGY PERSPECTIVE IF WE UNDERSTAND THERE ARE DIFFERENCES AND WE SEE, YOU KNOW, THERE'S A DRUG ACTIONABLE OR WHATEVER, IF WE CANNOT IMPLEMENT THAT FINDING, THIS IS FOR INTERVENTION AND BEHAVIORAL SCIENTISTS, WHERE THEY ARE
1:56:44
EXTREMELY IMPORTANT, THEN IT WILL NEVER REDUCE THE DISPARITY. UNDERSTANDING THE DISPARITY IS ONE THING BUT COMING UP WITH WAYS TO IMPLEMENT BOTH FINDINGS ARE MORE IMPORTANT IN TERMS OF THIS KIND OF WORK. THIS IS AN OLDISH FIGURE BUT I COME BACK TO IT AGAIN AND AGAIN, IT HIGHLIGHTS COMPLEXITY AND WHAT THE ROLE OF SCIENTISTS INCLUDING THOSE AT NIH CAN PLAY. I TALKED ABOUT WE WOULD SPEND A MOMENT TALKING ABOUT WHAT NEXT. THERE'S NO QUESTION THAT REVOLUTION IN TECHNOLOGY HAS
1:57:20
REALLY ENABLED US TO DELVE DEEPER INTO THE BIOLOGY OF THE DISPARITIES, AND TRY AND UNDERSTAND WHAT'S SIMILAR, WHAT'S DIFFERENT, WHAT'S ACTIONABLE, WHAT'S REPRODUCIBLE AND HOW CAN THE IT BETTER HELP OUR UNDERSTANDING OF BIOLOGY. WITH THAT SEVERAL GROUPS ACROSS THE UNITED STATES, THIS IS PUBLISHED A COUPLE -- ABOUT A MONTH OR TWO AGO, THE AACR, ASCO, ACS AND NCI TOOK A HARD LOOK AND SAID WHERE ARE WE NOW AND WHERE DO WE NEED TO GO AND OUTLINED SEVERAL THINGS THAT THEY THOUGHT AND I AGREE WITH
1:57:58
ARE IMPORTANT IN TERMS OF MOVING FORWARD. BRIEFLY A LOT OF THE WORK COMES BACK TO -- WE TALKED ABOUT THIS EARLIER, DEFINING AND IMPROVING DATA MEASURES FOR CANCER& DISPARITIES RESEARCH. YOU COULD PUT ANY EPIDEMIOLOGY RESEARCH DISCIPLINE AFTER THAT BECAUSE WE TALKED ABOUT SMOKING EARLIER. IF WE CAN'T ACCURATELY DEFINE EXPOSURE WE'RE TRYING TO MEASURE WE'RE NOT GOING TO HAVE A VERY REFINED AND EASILY UNDERSTANDABLE RESULT. BUT AGAIN IN TERMS OF DISPARITIES, THIS BECOMES PARTICULARLY IMPORTANT.
1:58:33
ONE ASPECT OF THAT, BUT CERTAINLY NOT THE ONLY, ONE ASPECT I TALKED ABOUT EARLIER IN TERMS OF MARKERS, TRYING TO UNDERSTAND THE ELEMENTS OF GENETIC ANCESTRY TO CONTRIBUTES TO DISPARITIES AND ALSO THE MORE ETHNIC RELATED FACTORS AS WELL. THAT'S ONE OF THE THINGS. THEY ALSO TALKED OF COURSE ABOUT ADDRESSING DISPARITIES IN CANCER INCIDENCE, CANCER SURVIVAL. A HUGE PART IS ACCESS TO CARE, THE ACCESS TO THE SAME CARE AND COMING UP WITH INTERVENTIONS, WAYS TO ENSURE THAT EVERYBODY
1:59:08
USES THE SAME CARE, IN THE SAME WAY. IN ADDITION, SOME WORK WE'RE DOING, IT ALSO -- THERE ARE SUGGESTIONS BIOLOGY IS ALSO IMPORTANT. AND I TALKED ABOUT THIS EARLIER TOO, TO REEMPHASIZE IMPROVING COMMUNITY ENGAGEMENT IN CANCER RESEARCH. IT'S A BROAD STATEMENT BUT IT GOES BACK AGAIN TO THE INTERVENTION. AND SO HPV IS ONE EXAMPLE, PHENOMENALLY SUCCESSFUL CANCER PREVENTION TOOL BUT IF PEOPLE DON'T USE IT IT'S NOT EFFECTIVE. FOR POPULATIONS THAT DON'T USE IT, TRYING TO UNDERSTAND WHY
1:59:42
THAT IS AND TRYING TO ENCOURAGE AND ENGAGE AND TRY TO INCREASE UPTAKE. THE LAST PART IS CONSIDERS REDESIGNING CLINICAL TRIALS TO ACKNOWLEDGE AND ADDRESS CANCER DISPARITIES. A COUPLE EXAMPLES, YOU PROBABLY KNOW ALREADY THAT THE PARTICIPATION OF AFRICAN-AMERICANS IN CLINICAL TRIALS IS VERY LOW, EVEN TO BEGIN WITH, RIGHT? BEFORE WE DO ANYTHING ELSE. THERE'S A LOT OF EFFORTS ONGOING TO UNDERSTAND WHY THAT IS THE CASE AND TRY TO COME UP WITH INTERVENTIONS TO IMPROVE IT. THE REASON THAT'S IMPORTANT IS
2:00:16
HOPEFULLY CLEAR. WE KNOW BIOLOGY IS DIFFERENT FOR MANY CANCERS, SO WE NEED TO ENSURE THAT AFRICAN-AMERICANS ARE APPROPRIATELY REPRESENTED, ANY RACIAL GROUP, SO IF THERE ARE DIFFERENCES IN OUTCOME OR RACE WE CAN ANALYZE. THE NCI HAS A RULE IF YOU CONDUCT AN NCI CLINICAL TRIAL YOU MUST IN YOUR ANALYSIS STRATIFY BY RACE TO SEE IF THERE ARE DIFFERENCES. THE PROBLEM IS POWER. IF YOU DON'T HAVE ENOUGH PEOPLE ENROLLED YOU WON'T BE ABLE TO FIND THE ANSWER. IT'S INCREDIBLY IMPORTANT, I'M
2:00:52
STRUCK WITH A TALK I WAS AT ACR LAST YEAR TALKING ABOUT IMMUNOTHERAPY, EVERYBODY IS TALKING ABOUT FOR GOOD RECENT DATA. PRESENTING THE RESULTS OF THE NEW ENGLAND JOURNAL PAPER, VERY DRAMATIC EFFECT IN LUNG CANCER AT THE TIME. OF COURSE I WAS SITTING THERE THINKING HOW DID IT WORK EQUALLY IN ALL POPULATIONS, FROM OTHER WORK WE DO, A SUGGESTION MAYBE IT WON'T IN EUROPEAN-AMERICANS AND AFRICAN-AMERICANS, I WAS CURIOUS. THERE WAS ONE AFRICAN-AMERICAN ENROLLED IN THE TRIAL.
2:01:21
YOU HAVE NO WAY TO ANSWER THE QUESTION. SO BECAUSE WE KNOW AFRICAN-AMERICANS ARE LESS LIKELY TO ENROLL IN TRIALS, BECAUSE WE KNOW BIOLOGY IS DIFFERENT AND WE KNOW THERE MAY BE DIFFERENTS IN OUTCOME, THERE'S AN ONUS FOR US AT A TIME WITH A MASSIVE REVOLUTION THAT CAN INCREASE, TUMORS THAT NEVER RESPONDED BEFORE THERE'S A LIKELIHOOD THEY WILL RESPOND, THERE'S AN ONUS TO INCREASE THERAPY IN PATIENTS, TO ASK THE QUESTION AT LEAST, AND SO THERE'S AGAIN THE WHOLE AREA TRYING TO THINK ABOUT THIS AREA,
2:01:57
AND IT IS EXCEPTIONALLY IMPORTANT FOR MANY OF THE REASONS I JUST DESCRIBED. I'M GOING TO FINISH THERE. THE LAST SLIDE RECAPITULATES WHAT I SAID. MY E E-MAIL ADDRESS IS AT THE BEGINNING. MY FOCUS IS LUNG CANCER BUT I HAVE COLLEAGUES THAT WORK IN OTHER AREAS AND I WOULD BE HAPPY TO REDIRECT YOU. 02:02:24.671,00:00:00.000 THANKS FOR YOUR ATTENTION.
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