Scientific Highlights

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All Cancers

Cancer Incidence Among Pesticide Applicators

To investigate the association of atrazine use with cancer risk, the authors utilized information from the Agricultural Health Study, a prospective cohort that includes 57,310 licensed pesticide applicators. They extended a previous analysis of this association with six additional years of follow-up and more than twice as many cancer cases. Overall, 36,357 (68%) of the pesticide applicators reported using atrazine, among which there were 3,146 cases of cancer. There was no increase among atrazine users in overall cancer risk or at most cancer sites among the higher lifetime use or intensity-weighted lifetime day exposure categories compared with the lowest exposure categories. Based on 29 exposed cases of thyroid cancer, there was a significant risk of this cancer in the second and fourth quartiles of intensity-weighted lifetime days. (Beane Freeman LE, Rusiecki JA, Hoppin JA, et al. Atrazine and cancer incidence among pesticide applicators in the Agricultural Health Study [1994–2007]. Environ Health Perspect 2011;119:1253–1259)

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All-Cause Mortality

Dietary Fiber Intake

To investigate the relationship of dietary fiber intake with total and cause-specific mortality, the authors examined data from the NIH-AARP Diet and Health Study, a prospective cohort study in which diet was assessed using a food-frequency questionnaire at baseline. A total of 20,126 deaths among men and 11,330 deaths among women were identified during the average nine years of follow-up. Fiber intake was associated with a lowered risk of total death (highest vs. lowest quintile: RR = 0.78 among both men and women). Fiber intake lowered the risk of death from cardiovascular, infectious, and respiratory diseases by 24% to 56% among men and by 34% to 59% among women. An inverse association between dietary fiber intake and cancer death was observed among men but not women. Fiber from grains, but not other sources, was significantly inversely related to total and cause-specific death among both men and women. (Park Y, Subar AF, Hollenbeck A, Schatzkin A. Dietary fiber intake and mortality in the NIH-AARP Diet and Health Study. Arch Intern Med 2011;171:1061–1068)

Waist Circumference, Body Mass Index, and Mortality

The authors evaluated the association of waist circumference (WC) and body mass index (BMI) with mortality using data from the NIH-AARP Diet and Health Study for 225,712 women and men. A total of 20,977 deaths were documented during follow-up from 1996 through 2005. Increased WC consistently predicted risk of death due to any cause as well as major causes of death, independent of BMI. WC was related to a 1.37-fold increased risk of death from any cancer and a 1.82-fold increased risk of death from cardiovascular disease, comparing the highest versus lowest WC categories. WC, but not BMI, showed significant positive associations with deaths from lung cancer and chronic respiratory disease. (Leitzmann MF, Moore SC, Koster A, et al. Waist circumference as compared with body-mass index in predicting mortality from specific causes. PLoS One 2011;6:e18582)

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Anal Cancer

HPV Vaccine Efficacy

To assess the efficacy of a bivalent HPV 16/HPV 18 vaccine against anal infection with HPV 16, HPV 18, or both, investigators performed an analysis within a cohort of Costa Rican women, ages 18–25, who were administered the vaccine as part of a randomized, controlled trial to determine its efficacy against persistent cervical HPV infections. At the final follow-up visit four years after vaccination, women who consented provided an anal specimen for a one-time assessment of vaccine efficacy against anal HPV 16/18 infection. The analyses were based on the full cohort of women who provided a specimen and a restricted cohort of women who were negative for both cervical HPV 16 and HPV 18 DNA and who were HPV 16 and HPV 18 seronegative before enrollment. In the full cohort, vaccine efficacy against prevalent HPV 16/18 infection was lower at the anus (62.0%) than at the cervix (76.4%; p for interaction by anatomical site = 0.031). In the restricted cohort, vaccine efficacy against anal HPV 16/18 infection was 83.6%, which was similar to vaccine efficacy against cervical HPV 16/18 infection (87.9%). These results demonstrate that the bivalent vaccine affords strong protection against anal HPV infection, particularly among women more likely to be HPV seronegative at enrollment. (Kreimer AR, González P, Katki HA, et al. Efficacy of a bivalent HPV 16/18 vaccine against anal HPV 16/18 infection among young women: A nested analysis within the Costa Rica Vaccine Trial. Lancet Oncol 2011;12:862–870)

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Bladder Cancer

Smoking and Bladder Cancer

The authors evaluated the association between tobacco smoking and bladder cancer among 281,394 men and 186,134 women in the NIH-AARP Diet and Health Study cohort who completed a lifestyle questionnaire. During follow-up, incident bladder cancer occurred among 3,896 men and 627 women (144.0 and 34.5 per 100,000 person-years, respectively). Former smokers (119.8 per 100,000 person-years; HR = 2.22) and current smokers (177.3 per 100,000 person-years; HR = 4.06) had higher risks of bladder cancer than never smokers. Compared with a pooled estimate of U.S. data from cohorts initiated between 1963 and 1987, RRs for smoking in the more recent NIH-AARP Diet and Health Study cohort were significantly higher, suggesting that recent changes in the composition of cigarettes and smoking practices (e.g., greater inhalation) are increasing the risks of bladder and perhaps other smoking-related cancers. (Freedman ND, Silverman DT, Hollenbeck AR, et al. Association between smoking and risk of bladder cancer among men and women. JAMA 2011;306:737–745)

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Breast Cancer

Breast Cancer Trends in the United States

To investigate U.S. time trends for the overall incidence of breast cancer and for estrogen receptor positive (ER+) and estrogen receptor negative (ER–) breast cancers, the authors developed a simple imputation method to correct invasive female breast cancer incidence for missing or unknown ER expression using data from the NCI SEER Program during 1980–2008. Corrected rates of ER+ and ER– breast cancers were used to calculate age-standardized incidence rates, estimated annual percent changes, and projections derived from age-period-cohort models. The incidence of breast cancer overall stabilized to near 200 per 100,000 woman-years by 2007–2008, reflecting a transient decrease in ER+ cancers and a steady decrease of ER– cancers (see Figure 1). The projected incidence rate for breast cancer overall through the year 2016 was similar to the incidence rate during 2007–2008. Rates of ER+ cancers were projected to increase 5.3% and rates of ER– breast cancers were projected to decrease 11.4% during 2009–2016. (Anderson WF, Katki HA, Rosenberg PS. Incidence of breast cancer in the United States: Current and future trends. J Natl Cancer Inst 2011;103:1397–1402)

Risk Factor Modification and Breast Cancer Risk

The authors developed a model to predict the absolute risk of breast cancer that included five nonmodifiable and three modifiable risk factors, using data from a case-control study of women in Italy (2,569 cases and 2,588 controls) and incidence and mortality data from the Florence Registries. The model was reasonably well calibrated (ratio of expected to observed cancers = 1.10, CI = 0.96–1.26), but the discriminatory accuracy was modest. The absolute risk reduction from exposure modifications was nearly proportional to the risk before the risk factors were modified and increased with age and risk projection time span. Mean 20-year reductions in absolute risk among women aged 65 years were 1.6% in the entire population, 3.2% among women with a positive family history of breast cancer, and 4.1% among women who accounted for the highest 10% of the total population risk. (Petracci E, Decarli A, Schairer C, et al. Risk factor modification and projections of absolute breast cancer risk. J Natl Cancer Inst 2011;103:1037–1048)

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Cervical Cancer

Vaccine Prevention Trial

The authors evaluated the efficacy of an HPV 16/18 vaccine against one-year persistent infection, stratified by age and sexual behavior in the Costa Rica Vaccine Trial, a community-based, randomized trial of 7,466 healthy women. According-to-protocol (ATP) cohorts included compliant HPV-negative women; intention-to-treat (ITT) included all randomized women. ATP vaccine efficacy was 90.9% against HPV 16/18 infection, 44.5% against HPV 31/33/45 infection, and 12.4% (CI = -3.2–25.6) against any oncogenic infection. Overall ITT vaccine efficacy against HPV 16/18 was 49.0%, but ATP and ITT vaccine efficacy reached almost 100% in year four of the follow-up. ATP efficacy against HPV 16/18 was similar by age, but ITT efficacy was highest among youngest women (68.9% among 18- to 19-year-olds; 21.8% among 24- to 25-year-olds) and 79.8% among virgins. Among previously unexposed women, vaccination was highly effective against HPV 16/18 and showed partial cross-protection against HPV 31/33/45. The benefit was maximal when vaccination was given to young women before initiation of sexual activity. (Herrero R, Wacholder S, Rodriguez AC, et al. Prevention of persistent human papillomavirus [HPV] infection by a HPV 16/18 vaccine: A community-based randomized clinical trial in Guanacaste, Costa Rica. Cancer Discov 2011; [E-pub ahead of print])

Number of Vaccine Doses

The authors evaluated the vaccine efficacy of fewer than three doses of an HPV 16/18 vaccine using data from the Costa Rica Vaccine Trial. Women were randomly assigned to receive three doses of the HPV 16/18 vaccine or a control vaccine and were followed for incident HPV 16 or HPV 18 infection that persisted in visits that were 10 or more months apart (median follow-up = 4.2 years). A total of 5,967 women received three vaccine doses (2,957 HPV, 3,010 control), 802 received two doses (422 HPV, 380 control), and 384 received one dose (196 HPV, 188 control). Incident HPV 16 or HPV 18 infections that persisted for one year were unrelated to dosage of the control vaccine. Vaccine efficacy was 80.9% for three doses of the HPV vaccine (CI = 71.1%–87.7%; 25 and 133 events in the HPV and control arms, respectively), 84.1% for two doses (CI = 50.2%–96.3%; 3 and 17 events), and 100% for one dose (CI = 66.5%–100%; 0 and 10 events). Four years after vaccination of women who appeared to be uninfected, this nonrandomized analysis suggests that two doses of the HPV 16/18 vaccine, and maybe even one dose, are as protective as three doses. (Kreimer AR, Rodriguez AC, Hildesheim A, et al. Proof-of-principle evaluation of the efficacy of fewer than three doses of a bivalent HPV16/18 vaccine. J Natl Cancer Inst 2011;103:1444–1451)

Concurrent Testing for HPV and Cervical Cytology

The authors assessed the five-year cumulative incidence, starting in 2003–2005, of cervical cancer and cervical intraepithelial neoplasia grade 3 (CIN 3) or worse among 331,818 women aged 30 years and older who enrolled in HPV/cervical cytology co-testing at Kaiser Permanente Northern California. Among 315,061 women negative by HPV testing, the five-year cumulative incidence of cancer was 3.8 per 100,000 women per year, which was slightly higher than that for the 306,969 women who were negative by both HPV and cervical cytology (3.2 per 100,000) and half the cancer risk of the 319,177 women who were negative by cervical cytology (7.5 per 100,000) (see Figure 2). Abnormal cytology greatly increased cumulative incidence of CIN 3 or worse over five years for the 16,757 women positive by HPV testing. Although statistically significant, abnormal cytology did not increase the five-year risk of CIN 3 or worse for women negative by HPV testing to a substantial level. The results indicate that for women aged 30 years and older in routine clinical practice who are negative by co-testing, three-year screening intervals in routine clinical practice are adequate because a single negative test for HPV is sufficient to assure against cervical cancer over five years. (Katki HA, Kinney WK, Fetterman B, et al. Cervical cancer risk for women undergoing concurrent testing for human papillomavirus and cervical cytology: A population-based study in routine clinical practice. Lancet Oncol 2011;12:663–672)

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Colorectal Cancer

Iron Homeostasis and Colorectal Adenoma

The authors conducted a case-control study within the PLCO Cancer Screening Trial to evaluate prospectively assessed dietary intake and serum measures of iron in relation to colorectal adenoma risk among 356 cases of colorectal adenoma and 396 polyp-free controls. Variation in eight genes involved in iron homeostasis was investigated among an additional 1,126 cases and 1,173 controls. A positive association was observed between red meat intake and colorectal adenoma (quartile 4 vs. quartile 1: OR = 1.59). Risk was inversely associated with serum total iron binding capacity and unsaturated iron binding capacity (quartile 4 vs. quartile 1: OR = 0.57 and OR = 0.62, respectively). However, there was no association with serum ferritin, iron, or transferrin saturation or with polymorphisms in genes involved in iron homeostasis. (Cross AJ, Sinha R, Wood RJ, et al. Iron homeostasis and distal colorectal adenoma risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Cancer Prev Res [Phila] 2011;4:1465–1475)

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Familial Cancer

Confirmation of Family Cancer History

In the population-based Connecticut Family Health Study, participants reported cancer in 20,578 first-degree relatives (FDR) and second-degree relatives (SDR). Of those, 2,605 relatives were sampled for confirmation of reports on breast, colorectal, prostate, and lung cancer from state cancer registries, Medicare databases, the National Death Index, death certificates, and health care facility records. Sensitivity and positive predictive value were low to moderate and varied by cancer type: 60.2% and 40.0%, respectively, for lung cancer; 27.3% and 53.5% for colorectal cancer; 61.1% and 61.3% for breast cancer; and 32.0% and 53.4% for prostate cancer. Specificity and negative predictive value were higher than 95% for all four cancer types. Cancer history reports for FDR were more accurate than reports for SDR. Efforts to improve accuracy are needed in settings where family history is collected to ensure appropriate risk assessment and clinical care recommendations. (Mai PL, Garceau AO, Graubard BI, et al. Confirmation of family cancer history reported in a population-based survey. J Natl Cancer Inst 2011;103:788–797)

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Gastric Cancer

Serum Ghrelin Concentration

The authors evaluated serum levels of the hormone ghrelin among 261 gastric noncardia adenocarcinoma (GNCA) patients, 98 esophagogastric junctional adenocarcinoma (EGJA) patients, and 441 control subjects in the prospective Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Risks of both GNCA and EGJA were increased for individuals in the lowest quartile of serum ghrelin compared with those in the highest quartile (GNCA: OR = 5.63; EGJA: OR = 4.90). These results suggest a potential role for gastric hormones in carcinogenesis. (Murphy G, Kamangar F, Dawsey SM, et al. The relationship between serum ghrelin and the risk of gastric and esophagogastric junctional adenocarcinomas. J Natl Cancer Inst 2011;103:1123–1129)

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Liver Cancer

Metabolic Syndrome and Liver Cancer

The authors evaluated the prevalence of metabolic syndrome and other risk factors for hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) among 3,649 HCC and 743 ICC cases diagnosed between 1993 and 2005 in the SEER-Medicare database and among a 5% sample of individuals (195,953 persons) residing in the same SEER regions as the case subjects. Metabolic syndrome was significantly more common among persons who developed HCC (37.1%) or ICC (29.7%) than among the comparison group (17.1%). In adjusted multiple logistic regression analyses, metabolic syndrome remained significantly associated with increased risk of HCC (OR = 2.13) and ICC (OR = 1.56). (Welzel TM, Graubard BI, Zeuzem S, et al. Metabolic syndrome increases the risk of primary liver cancer in the United States: A study in the SEER-Medicare database. Hepatology 2011;54:463–471)

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Lung Cancer

Circulating Cytokines and Lung Cancer

The authors analyzed circulating cytokines as inflammation biomarkers among 270 lung cancer cases and 296 controls in the NCI-Maryland case-control study. Results were validated among 532 cases and 595 controls in the prospective PLCO Cancer Screening Trial. Serum IL-6 and IL-8 levels were associated with lung cancer risk in both the NCI-Maryland study (IL-6: OR = 3.29; IL-8: OR = 2.06) and the PLCO study (IL-6: OR = 1.48, CI = 1.04–2.10; IL-8: OR = 1.57), comparing the highest to the lowest quartiles. In the PLCO study, increased IL-6 levels were associated only with lung cancer diagnosed within two years of blood collection, whereas increased IL-8 levels were associated with cancer diagnosed more than two years after blood collection. The 10-year standardized absolute risk (AR) of lung cancer in the PLCO study was highest among current smokers with high IL-8 and C-reactive protein levels (AR = 8.01%). (Pine SR, Mechanic LE, Enewold L, et al. Increased levels of circulating interleukin 6, interleukin 8, C-reactive protein, and risk of lung cancer. J Natl Cancer Inst 2011;103:1112–1122)

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Lymphoma

Immune Markers and Non-Hodgkin Lymphoma

In a nested case control study within the PLCO Cancer Screening Trial, selected cytokines (IL-4, IL-6, IL-10, and TNF-α) and other immune markers (soluble TNF receptor 1 [sTNF-R1], sTNF-R2, C-reactive protein, and sCD27) were measured in prediagnostic serum specimens from 297 incident non-Hodgkin lymphoma (NHL) cases and 297 controls. NHL risk was significantly associated with elevated serum levels of sTNF-R1 (quartile 4 vs. quartile 1: OR = 1.7) and sCD27 (OR = 5.3). These associations persisted in analyses based on cases diagnosed longer than six years following blood collection. Elevated levels of IL-10, TNF-α, and sTNF-R2 were also significantly associated with increased risk of NHL; however, these associations weakened with increasing time from blood collection to case diagnosis and were null for cases diagnosed more than six years after collection. The findings support a role for subclinical inflammation and chronic B-cell stimulation in lymphomagenesis. (Purdue MP, Lan Q, Bagni R, et al. Prediagnostic serum levels of cytokines and other immune markers and risk of non-Hodgkin lymphoma. Cancer Res 2011;71:4898–4907)

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Osteosarcoma

Genetic Variation Associated with Osteosarcoma

To understand the contribution of genes involved in DNA repair, ribosomal function, growth/hormone, and bone formation to osteosarcoma (OS) pathogenesis, the authors evaluated 4,836 tag-SNPs across 255 candidate genes among 96 OS cases and 1,426 controls. Twelve SNPs in growth or DNA repair genes were significantly associated with OS, including four SNPs in the DNA repair gene FANCM and two SNPs downstream of the growth hormone gene GH1. One SNP in the region of each of the following genes was significant: MDM2, MPG, FGF2, FGFR3, GNRH2, and IGF1. The results indicate that several SNPs in biologically plausible pathways are associated with the risk of OS. (Mirabello L, Yu K, Berndt SI, et al. A comprehensive candidate gene approach identifies genetic variation associated with osteosarcoma. BMC Cancer 2011;11:209)

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Pancreatic Cancer

Advanced Glycation End Products and Pancreatic Cancer Etiology

The authors examined prediagnostic measures of N^ε-(carboxymethyl)-lysine (CML)-advanced glycation end products (AGEs) and soluble receptors for AGEs (sRAGE) with pancreatic cancer in 29,133 Finnish male smokers within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. CML-AGE, sRAGE, glucose, and insulin concentrations were measured in fasting serum from 255 incident pancreatic cancer cases and from 485 randomly sampled subcohort participants. CML-AGE levels were not associated with pancreatic cancer (fifth quintile vs. first quintile: RR = 0.68, CI = 0.38–1.22). In contrast, sRAGE levels were inversely associated with pancreatic cancer (fifth quintile vs. first quintile: RR = 0.46, CI = 0.23–0.73). Further adjustment for glucose or insulin levels did not change the observed associations. (Jiao L, Weinstein SJ, Albanes D, et al. Evidence that serum levels of the soluble receptor for advanced glycation end products are inversely associated with pancreatic cancer risk: A prospective study. Cancer Res 2011;71:3582–3589)

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Prostate Cancer

Fine Mapping Chromosome 11q13

Genome-wide association studies have identified prostate cancer susceptibility alleles on chromosome 11q13. As a part of the Cancer Genetic Markers of Susceptibility initiative, the authors fine mapped the region flanking the most significant marker, rs10896449, among 10,272 prostate cancer cases and 9,123 controls using 120 common SNPs selected by a two-staged tagging strategy. Single-locus analysis identified 18 SNPs below genome-wide significance, with rs10896449 being the most significant (p = 7.97 × 10^-19). Multi-locus models identified a second association at rs12793759 (OR = 1.14, p = 4.76 × 10^-5) that was independent of rs10896449. A third detected association, rs10896438, was independent of both rs10896449 and rs12793759 (OR = 1.07, p = 5.92 × 10^-3). The observation of a recombination hotspot that separates rs10896438 from rs10896449 and rs12793759 as well as low linkage disequilibrium corroborates the finding of three independent signals (see Figure 3). (Chung CC, Ciampa J, Yeager M, et al. Fine mapping of a region of chromosome 11q13 reveals multiple independent loci associated with risk of prostate cancer. Hum Mol Genet 2011;20:2869–2878)

Fine Mapping Chromosome 19q13.33

Germline variants in the gene that encodes the prostate-specific antigen (PSA) protein (KLK3) have been associated with serum PSA levels and prostate cancer. The authors fine mapped the KLK3 locus by genotyping tag SNPs among 3,522 prostate cancer cases and 3,338 controls from five case-control studies. The authors did not observe a strong association between the KLK3 variant and prostate cancer risk, but three highly correlated SNPs (rs17632542, rs62113212, and rs62113214) were associated with prostate cancer (OR = 0.77, CI = 0.67–0.89, p = 3.41 × 10^-4). The signal was apparent only for nonaggressive prostate cancer cases with Gleason score < 7 and disease stage < III. Baseline PSA levels were 43.7% higher in controls with no minor alleles than in controls with one or more minor alleles at any one of the three SNPs. The results suggest that germline KLK3 variants may influence the diagnosis of nonaggressive prostate cancer by influencing serum PSA levels and subsequent likelihood of biopsy. (Parikh H, Wang Z, Pettigrew KA, et al. Fine mapping the KLK3 locus on chromosome 19q13.33 associated with prostate cancer susceptibility and PSA levels. Hum Genet 2011;129:675–685)

Gene-Gene Interactions and Prostate Cancer

The authors used data from the Cancer Genetic Markers of Susceptibility program to explore possible interactions between known prostate cancer susceptibility loci and SNPs. Stage I included 523,841 SNPs in 1,175 cases and 1,100 controls. Stage II included 27,383 SNPs in an additional 3,941 cases and 3,964 controls. Several noteworthy interacting SNP pairs were identified through empirical Bayes analysis, although none reached genome-wide significance. An interaction was found between the major prostate cancer susceptibility locus in the subregion of 8q24 that contains POU5F1B and an intronic SNP in the transcription factor EPAS1, which has potentially important functional implications for 8q24. Another noteworthy result involved interaction of a known prostate cancer susceptibility marker near the prostate protease genes KLK2 and KLK3 with an intronic SNP in PRXX2.. (Ciampa J, Yeager M, Amundadottir L, et al. Large-scale exploration of gene-gene interactions in prostate cancer using a multistage genome-wide association study. Cancer Res 2011;71:3287–3295)

Serum Retinol and Prostate Cancer

The authors used high-performance liquid chromatography to measure serum retinol levels from men in the prospective Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort at baseline (n = 29,104) and after three years (n = 22,843). Men with higher retinol concentrations at baseline were more likely to develop prostate cancer (quintile 5 vs. quintile 1: HR = 1.19), and results were similar for aggressive disease. Men who were in the highest quintile for retinol levels at baseline and after three years had the greatest increased risk (HR = 1.31). (Mondul AM, Watters JL, Männistö S, et al. Serum retinol and risk of prostate cancer. Am J Epidemiol 2011;173:813–821)

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Testicular Cancer

Adult Height and Testicular Cancer

The authors genotyped 15 height-related SNPs among 561 cases and 676 controls in the U.S. Servicemen's Testicular Tumor Environmental and Endocrine Determinants case-control study. Two SNPs were found to be associated with risk of testicular germ cell tumors (TGCT): rs6060373 (CC vs. TT: OR = 1.51) and rs143384 (CC vs. TT: OR = 1.53). No individual SNP attenuated the association between height and TGCT. (Cook MB, Chia VM, Berndt SI, et al. Genetic contributions to the association between adult height and testicular germ cell tumors. Int J Epidemiol 2011;40:731–739)

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Thyroid Cancer

Dietary Nitrate and Nitrite

To assess whether dietary nitrate and nitrite are associated with thyroid cancer risk overall and by subtype, the investigators used data from the NIH-AARP Diet and Health Study, a prospective cohort of 490,194 men and women ages 50–71 years in 1995–1996. Dietary intakes were assessed using a food frequency questionnaire. After an average of seven years of follow-up, 370 incident thyroid cancer cases with complete dietary information were identified. Among men, increasing nitrate intake was positively associated with thyroid cancer risk (highest vs. lowest quintile: RR = 2.28); however, no trend was observed among women. Nitrite intake was not associated with overall risk of thyroid cancer among either men or women. Positive associations were found between nitrate intake and both papillary (RR = 2.10) and follicular thyroid cancer (RR = 3.42) among men, while nitrite intake was positively associated with follicular thyroid cancer (RR = 2.74) among men. These results support a role of nitrate in thyroid cancer risk. (Kilfoy BA, Zhang Y, Park Y, et al. Dietary nitrate and nitrite and the risk of thyroid cancer in the NIH-AARP Diet and Health Study. Int J Cancer 2011;129:160–172)

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