In 1946, the Society’s Research Department began with Extramural Grants and what was then called the Epidemiology Department, which later changed its name to the Department of Epidemiology and Surveillance Research. To enhance the productivity of this area of research, a re-organization and name change for the former Department of Epidemiology and Surveillance Research resulted in two independent research departments in early FY2009. The former department consisted of two functionally separate components of epidemiology research representing both analytic epidemiology and surveillance research, which also housed health services research. The two new departments are (1) Surveillance and Health Policy Research, with Elizabeth Ward, PhD as its vice president, and (2) Epidemiology, with Susan Gapstur, PhD, MPH as its new vice president. Vice President Michael Thun, MD, MS of the former combined department, has become the Vice President Emeritus, Epidemiology and Surveillance. All three vice presidents report directly to the new National Vice President of Research, who, as of January 2009, is Dr. Victor Vogel.

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Cancer Prevention Study II

The Cancer Prevention Study II (CPS-II), which began in 1982, is a prospective mortality study of approximately 1.2 million American men and women. Approximately 77,000 volunteers for the American Cancer Society recruited participants into the study in all 50 states, the District of Columbia, and Puerto Rico.

Each participant completed a four-page, confidential questionnaire. Baseline questions included personal identifiers, height, weight, demographic characteristics, personal and family history of cancer and other diseases, use of medicines and vitamins, menstrual and reproductive history (women), occupational exposures, dietary habits, alcohol and tobacco use, and various questions regarding exercise and behavior.

During the 24 years of completed mortality follow-up currently available for this cohort (1982-2006), 491,188 deaths have occurred; cause of death has been obtained for 99.3% of all deaths. Follow-up of CPS-II is expected to continue for many years to maximize the information obtained from this valuable study.

CPS-II Nutrition Survey

The CPS-II Nutrition Survey cohort was established in 1992 and 1993 as a subset of the larger CPS-II cohort with two primary objectives: 1) to obtain detailed information on dietary exposures and to update with additional exposure information, and 2) to conduct prospective cancer incidence follow-up in addition to mortality follow-up.

With these objectives in mind, staff again contacted close to half of the CPS-II population (men and women ages 50-74 in 21 states) in 1992 and 1993 and obtained updated information on nutrition and other cancer risk factors for 184,194 men and women. The 21 states participating in this survey were California, Connecticut, Florida, Georgia, Illinois, Iowa, Louisiana, Maryland, Massachusetts, Michigan, Minnesota, Missouri, New Mexico, New Jersey, New York, North Carolina, Pennsylvania, Utah, Virginia, Washington, and Wisconsin.

New questionnaires were sent to the CPS-II Nutrition Survey cohort in 1997, 1999, 2001, 2003, 2005, and 2007. These questionnaires updated information on exposures and also captured self-reported cancer incidence.

Ongoing cancer incidence follow-up for the CPS-II Nutrition Survey cohort is conducted by validating self-reported incidence cancers using medical records or linkage with state cancer registries. Nearly 30,000 incident cancers were reported in the interval 1992 to 2005. These data are used to examine the association of many factors (e.g., diet, lifestyle, and environment) with cancer incidence. Mortality follow-up of the entire CPS-II Nutrition Survey cohort will allow the study of the association between reported risk factors and survival. Initial findings include marked associations between obesity and aggressive forms of prostate cancer.

CPS-II Biorepository (addition of blood and cheek cell samples to CPS-II)

The Society has collected and archived blood samples from 40,000 participants and cheek cell samples (as a source of DNA) from 70,000 participants in the CPS-II Nutrition Survey cohort. The addition of archived biological specimens to the questionnaire information provided by the same individuals will provide a valuable long-term resource for examining many scientific questions, including how nutritional factors, hormones, and genetic susceptibility affect cancer risk. In separate collaborations with the Cancer Genetic Markers of Susceptibility (CGEMS) initiative and with the Breast and Prostate Cancer Cohort consortium (BPC3), inherited variations that increase the risk for breast and prostate cancer were recently described. Further analysis of other genetic information collected is ongoing.

Cancer Prevention Study-3 (CPS-3)

The Society’s Epidemiology and Surveillance Research program is inviting men and women between the ages of 30 and 65 years who have no personal history of cancer to join a historic research study. The ultimate goal is to enroll 500,000 adults from various racial/ethnic backgrounds from across the United States. The purpose of Cancer Prevention Study-3 (CPS-3) is to better understand ways to prevent cancer. This multi-year survey will study lifestyle, behavioral, environmental and genetic factors that may cause or prevent cancer with the ultimate goal of eliminating cancer as a major health problem for this and future generations.

Study enrollment took place at select Relay For Life® events in local communities. CPS Cancer Prevention Study-3 (CPS-3) is a grassroots effort in which Relay participants from across the country can contribute to cancer research not only through their fund-raising efforts, but also by participating actively in research.

Information about Cancer Prevention Study-3 (CPS-3) and any upcoming Relay For Life® events where future enrollment will be held is provided at www.cancer.org/cps3.

Ongoing Analyses

The staff of Epidemiology and Surveillance Research is currently conducting analyses using data from CPS-II and the CPS-II Nutrition Survey. These include analyses of diet, hormones, physical activity, vitamin use, and other risk factors for selected common cancers, and updated dose-response analyses between smoking and mortality. Collaborative studies are under way with the National Cancer Institute, the Centers for Disease Control and Prevention, Harvard University, and several other universities.

Epidemiology Publications, Fiscal Year 2008
From CPS-II and CPS-II Nutrition Survey:
1. Calle EE, Feigelson HS, Thun MJ, Rodriguez C. Cancer Genetics Markers of Susceptibility. Multiple novel loci identified in a genome-wide association study of prostate cancer. Nature Genetics. 2008;40:310-5. This report is a genome-wide association study on cases of prostate cancer.

2. Chen J, Rodriguez C. Conditional likelihood methods for haplotype-based association analysis using matched case-control data. Biometrics. 2007;63(4):1099-107. We study two conditional likelihood approaches that address the issue that haplotypes cannot be inferred with certainty from SNP genotype data. The approach based on the likelihood of disease status conditioned on the total number of cases, genotypes, and other covariates within each matching stratum was more robust to model assumptions on the diplotype distribution conditioned on environmental risk variables and matching factors in the control population.

3. Danforth KN, Hayes RB, Rodriguez C, Sakoda LC, Huang WY, Yu K, Chen BE, Chen J, Andriole GL, Calle EE, Jacobs EJ, Chu LW, Figueroa JD, Yeager M, Platz EA, Michaud DS, Chanock SJ, Thun MJ, Hsing AW. Polymorphic variants in PTGS2 and prostate cancer risk: Results from two large nested case-control studies. Carcinogenesis. 2008;29(3):568-72. Despite the potential importance of inflammation in prostate carcinogenesis results from our large study of 5 PTGS2 SNPs does not support a strong association between PTGS2 variants and prostate cancer risk.

4. Danforth KN, Rodriguez C, Hayes RB, Sakoda LC, Huang WY, Yu K, Calle EE, Jacobs EJ, Chen BE, Andriole GL, Figueroa JD, Yeager M, Platz EA, Michaud DS, Chanock SJ, Thun MJ, Hsing AW. TNF polymorphisms and prostate cancer risk. The Prostate. 2008;68(4):400-7. Intra-prostatic inflammation has been implicated in prostate cancer development. We investigated the association between 5 PTGS2 SNPs and prostate cancer risk in the PLCO Cancer Screening Trial and CPS-II. Results do not support a strong association among non-Hispanic white men.

5. Dong XY, Rodriguez C, Guo P, Sun X, Talbot JT, Zhou W, Petros J, Li Q, Vessella RL, Kibel AS, Stevens VL, Calle EE, Dong JT. SnoRNA U50 is a candidate tumor suppressor gene at 6q14.3 with a mutation associated with clinically significant prostate cancer. Hum Mol Genet. 2008;17(7):1031-42. A homozygous 2-bp deletion in the U50 gene was detected both somatically and in germline in 11 of 119 prostate cancer samples, but not in any of 104 normal controls, whereas a heterozygous genotype occurred at similar rates between cancer and controls. Analysis of prostate cancer and controls from the CPS-II Nutrition Cohort showed that homozygous genotype of the deletion predicted prostate cancer.

6. Feigelson HS, Calle EE, Rodriguez C, Thun MJ. The Breast and Prostate Cancer Cohort Consortium. Sequence variants of estrogen receptor beta and risk of prostate cancer in the NCI BPC3. Cancer Epidemiol Biomarkers Prev. 2007;16(10):1973-81. There is little evidence that genetic variation in ESR2 contributes substantially to prostate cancer risk among white men.

7. Feigelson HS, Calle EE, Thun MJ. The Breast and Prostate Cancer Cohort Consortium. Haplotypes of the estrogen receptor beta (ESR2) gene and breast cancer risk. Int J Cancer. 2008;122(2):387-92. ESR2 variation may confer a small increased risk for postmenopausal.

8. Feigelson HS, Calle EE, Thun MJ. The Breast and Prostate Cancer Cohort Consortium. CYP17 genetic variation and risk of breast and prostate cancer from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium (BPC3). Cancer Epidemiol Biomarkers Prev. 2007;16(11):2237-46. Variation in CYP17 is not associated with risk of breast or prostate cancer.

9. Feigelson HS, Teras LR, Diver WR, Tang W, Patel AV, Stevens V, Calle EE, Thun MJ, Bouzyk M. Genetic variation in candidate obesity genes ADRB2, ADRB3, GHRL, HSD11B1, IRS1, IRS2, and SHC1 and risk for breast cancer in the Cancer Prevention Study II. Breast Cancer Res. 2008;10:R57. Genetic variation in the genes IRS2 and HSDIIBI may be associated with breast cancer risk. Five other genes (ADRB2, ADRB3, GHRL, IRSI and SHC1) were not associated with breast cancer.

10. Jacobs EJ, Hsing AW, Bain EB, Stevens VL, Wang Y, Chen J, Chanock SJ, Zheng SL, Xu J, Thun MJ, Calle EE, Rodriguez C. Polymorphisms in angiogenesis-related genes and prostate cancer. Cancer Epidemiol Biomarkers Prev. 2008;17(4):972-7. None of the 58 SNP's in angiogenesis-related candidate genes appeared likely to be importantly associated with risk of overall or advanced prostate cancer.

11. Jacobs EJ, Rodriguez C, Bain EB, Wang Y, Thun MJ, Calle EE. Cholesterol-lowering drugs and advanced prostate cancer incidence in a large U.S. cohort. Cancer Epidemiol Biomarkers Prev. 2007;16(11):2213-7 Results provide some support for the hypothesis that long-term statin use is associated with reduced risk of advanced prostate cancer.

12. Koushik A, McCullough M, Calle EE. Pooling project of prospective studies of fruits and vegetables and colon cancer risk. A pooled analysis of 14 cohort studies. J Natl Cancer Inst. 2007;99:1471-83. Fruit and vegetable intakes were not strongly associated with colon cancer risk overall, but may be associated with a lower risk of distal colon cancer.

13. McCullough M, Patel A, Patel R, Rodriguez C, Feigelson H, Bandera E, Gansler T, Thun M, Calle E. Body mass and endometrial cancer risk by hormone replacement therapy and cancer subtype. Cancer Epidemiol Biomarkers Prev. 2008;17(1):73-9 Greater BMI increased risk of cancer in never users of postmenopausal hormone therapy, but not in ever users.

14. Morozova N, Weisskopf MG, McCullough ML, Munger KL, Calle EE, Thun MJ, Ascherio A. Diet and amyotrophic lateral sclerosis. Epidemiology. 2008;19(2):324-37. This was the first prospective study to examine the association between diet and risk of ALS. After adjusting for multiple comparisons, diet did not appear to influence risk.

15. Patel AV, Feigelson HS, Talbot JT, McCullough ML, Rodriguez C, Patel RC, Thun MJ, Calle EE. The role of body weight in the relationship between physical activity and risk of endometrial cancer: Results from a large cohort of US women. Int J Cancer. 2008;123:1877-82. Light and moderate physical activity including daily life activities were associated with lower endometrial cancer risk in the Cancer Prevention Study-II Nutrition Cohort, a large prospective cohort study of US men and women. This inverse association was strongest among women who are overweight or obese.

16. Patel AV, Thun MJ, Calle EE, Feigelson HS. The Breast and Prostate Cancer Cohort Consortium. IGF-1, IGFBP-1, and IGFBP-3 polymorphisms predict circulating IGF levels but not breast cancer risk: Findings from the Breast and Prostate Cancer Cohort Consortium (BPC3), PLoS ONE. 2008;3(7):e2578. In a large pooled study of more than 6,000 predominantly Caucasian breast cancer cases and controls, the impact of genetic variation in IGF1 and IGFBP3 on circulating IGF levels did not appear to substantially influence breast cancer risk.

17. Rodriguez C, Feigelson HS, Deka A, Patel AV, Jacobs EJ, Thun MJ, Calle EE. Postmenopausal hormone therapy and lung cancer risk in the Cancer Prevention Study II Nutrition Cohort. Cancer Epidemiol Biomarkers Prev. 2008;17(3):655-60. In this study, current use of postmenopausal hormone therapy was significantly associated with 27% decreased risk of incident lung cancer. These results support the hypothesis that postmenopausal hormone therapy is associated with reduced risk of lung cancer; however, the absence of dose-response relationship weakens the evidence for causality.

18. Rodriguez C, Patel AV. Pooling Project of Diet and Cancer Cohorts. Height, Body Mass Index, and Ovarian Cancer: A Pooled Analysis of 12 Cohort Studies. Cancer Epidemiol Biomarkers Prev. 2008;17(4) 902-12. In this pooled analysis of 12 large prospective cohorts, height was associated with an increased ovarian cancer risk, especially in premenopausal women. BMI was not associated with ovarian cancer risk in postmenopausal women but was positively associated with risk in premenopausal women.

19. Stevens VL, Rodriguez C, Talbot JT, Pavluck AL, Thun MJ, Calle EE. Paraoxonase 1 (PON 1), polymorphisms and prostate cancer in the CPS-II Nutrition Cohort. The Prostate. 2008; 68:1336-40. The association of 2 nonsynonymous SNPs in PON1 and prostate cancer risk was investigated.

20. Thacker EL, Chen H, Patel AV, McCullough ML, Calle EE, Thun MJ, Schwarschild MA, Ascherio A. Recreational physical activity and risk of Parkinson's disease. Movement Disorders. 2008;23(1):69-74. In summary, the results of our study favor a role for physical activity in the prevention of PD, and other prospective epidemiological studies on this topic have been reasonably consistent.

21. Wang Y, Jacobs EJ, Patel AV, Rodriguez C, McCullough ML, Thun MJ, Calle EE. A prospective study of waist circumference and body mass index in relation to colorectal cancer incidence. Cancer Causes Control. 2008;19(7):783-92. Waist circumference was associated with increased colorectal cancer incidence, possibly partially independent of BMI. Other:

22. Bandera EV, Kushi LH, Moore DF, Gifkins DM, McCullough M. Dietary lipids and endometrial cancer: the current epidemiologic evidence. Cancer Causes Control. 2007;18(7):687-703 Meta-analysis of case-control data suggest an increased risk of endometrial cancer with greater total fat, saturated fat, and animal fat consumption. However, the limited available cohort data do not support these associations. Additional data, particularly from prospective studies, are needed before conclusions can be drawn regarding the association between dietary lipids and endometrial cancer.

23. Bandera EV, Kushi LH, Moore DF, Gifkins DM, McCullough ML. Consumption of animal foods and endometrial cancer risk: a systematic literature review and meta-analysis. Cancer Causes Control. 2007;18(9):967-88. This systematic literature review and meta-analysis found that red meat increases the risk of endometrial cancer.

24. Banez LL, Hamilton RJ, Partin AW, Vollmer RT, Sun L, Rodriguez C, Wang Y, Terris MK, Aronson WJ, Presti JC, Kane CJ, Amling CL, Moul JW, Freedland SJ. Obesity-related plasma hemodilution and PSA concentration among men with prostate cancer. JAMA. 2007;298:2275-80. Retrospective study of men who underwent radical prostatectomy for prostate adenocarcinoma from 1988 to 2006. In men undergoing radical prostatectomy, higher BMI was associated with higher plasma volume; hemodilution may therefore be responsible for the lower serum PSA concentrations among obese men with prostate cancer.

25. Calle EE. Obesity and Cancer. BMJ. 2007;335(7630):1107-8. Editorial comment on a paper from the UK Million Women Study describing associations between BMI and cancer incidence and mortality

26. Calle EE, Rodriguez R. Collaborative Group on Epidemiological Studies of Ovarian Cancer. Ovarian cancer and oral contraceptives: collaborative reanalysis of data from 45 epidemiological studies including 23257 women with ovarian cancer and 87,303 controls. Lancet. 2008;371:303-14. Use of oral contraceptives confers long-term protection against ovarian cancer. These findings suggest that oral contraceptives have already prevented some 200,000 ovarian cancers and 100,000 deaths from the disease, and that over the next few decades the number of cancers prevented will rise to at least 30 000 per year.

27. Fung TT, Chiuve SE, McCullough ML, Hu F. Adherence to a dash-style diet and risk of coronary heart disease and stroke. Arch Intern Med. 2008;168(7):713-20. The Dietary Approaches to Stop Hypertension (DASH) diet has been shown to lower blood pressure, but little is known about its long-term effect on cardiovascular end points. Our objective was to assess the association between a DASH-style diet adherence score and risk of coronary heart disease (CHD) and stroke in women.

28. Hawthorne MA, Hannan LM, Thun MJ, Samet JM. Protecting our children from second-hand smoke. UICC. 2008. This pamphlet presents an overview of the prevalence and health consequences of second-hand smoke exposure among children; details current interventions and policies aimed at reducing such exposure and provides recommendations for further legislative and educational efforts.

29. McCullough ML, Bandera EV, Moore DF, Kushi LH. Vitamin D calcium intake and endometrial cancer; a systematic review of the literature. Prev Med. 2008;46:298-302. This review summarizes work done as part of the WCRF/AICR review. Calcium, but not vitamin D intake, is related to lower risk of endometrial cancer in the few studies available for review.

30. Samet JM, Thun MJ, de Gonzales AB. Models of smoking and lung cancer risk: a means to an end. Epidemiology. 2007;18(5):649-51. This editorial paper provides a broad overview of the value and uses of models of lung cancer risk in relation to various parameters of smoking behavior.

31. Sedjo RL, Byers T, Barrera E, Cohen C, Fontham ET, Newman LA, Runowicz CD, Thorson AG, Thun MJ, Ward EM, Wender RC, Eyre HJ. A midpoint assessment of the American Cancer Society challenge goal to decrease cancer incidence by 25% between 1992 and 2015. CA Cancer J Clin. 2007;57:326-40. Between now and 2015, many more cancer deaths can be averted by concerted action to control tobacco and obesity, by redoubling efforts in mammography and colorectal cancer screening, and by enacting policies to close gaps in access to cancer detection and treatment.

32. Stevens VL, Patel AV, Feigelson HS, Rodriguez C, Thun MJ, Calle EE. Cryopreservation of whole blood samples collected in the field for a large epidemiologic study. Cancer Epidemiol Biomarkers Prev. 2007;16(10):2160-3. The paper describes the protocol used to collect and cryopreserve whole blood samples as well as the testing of these samples to determine the success of the protocol.

33. Thompson RL, Bandera EV, Burley VJ, Cade JE, Forman D, Freudenheim JL, Greenwood D, Jacobs DR, Kalliecharan RV, Kushi LH, McCullough ML, Miles LM, Moore DF, Moreton JA, Rastogi T, Wiseman MJ. Reproducibility of systematic literature reviews on food, nutrition, physical activity and endometrial cancer. Public Health Nutr. 2008;11(10):1006-14. This paper describes the process and reproducibility of the systematic literature review procedures used in the WCRF/AICR 2007 review.*

34. Thun MJ, Hannan LM, Stefanek M. Risky Business: Tools to Improve Risk Communication in a Doctor's Office. J Natl Cancer Inst. 2008;100:830-1. Editorial in response to Woloshin, et al., J Natl Cancer Inst, 2008, regarding risk communication and its possible implications.

35. Willett WC, McCullough ML. Dietary pattern analysis for the evaluation of dietary guidelines. Asia Pac J Clin Nutr. 2008;17(SI):75-8. This review discusses the need for and methods to evaluate efficacy of dietary guidelines empirically.

*Articles published online prior to the close of the fiscal year, but published in print after the close the fiscal year.