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We examined associations between two forms of testosterone therapy (TT) and risks of seven cancers among men.SEER-Medicare combines cancer registry data from the Surveillance, Epidemiology, and End Results programme with Medicare claims. Our population-based case-control study included incident cancer cases diagnosed between 1992-2015: prostate (n = 130,713), lung (n = 105,466), colorectal (n = 56,433), bladder (n = 38,873), non-Hodgkin lymphoma (n = 17,854), melanoma (n = 14,241), and oesophageal (n = 9116). We selected 100,000 controls from a 5% random sample of Medicare beneficiaries and used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI).TT was associated with lower risk of distant-stage prostate cancer (injection/implantation OR = 0.72, 95% CI: 0.60-0.86; topical OR = 0.50, 95% CI: 0.24-1.03). We also observed inverse associations for distant-stage colorectal cancer (injection/implantation OR = 0.75, 95% CI: 0.62-0.90; topical OR = 0.11, 95% CI: 0.05-0.24). Risks of distant-stage colorectal and prostate cancers decreased with time after initiating TT by injection/implantation. By contrast, TT was positively associated with distant-stage melanoma (injection/implantation OR = 1.70, 95% CI: 1.37-2.11). TT was not associated with bladder cancer, oesophageal cancer, lung cancer or non-Hodgkin lymphoma.TT was inversely associated with distant-stage prostate and colorectal cancers but was positively associated with distant-stage melanoma. These observations may suggest an aetiologic role for TT or the presence of residual confounding.

Prostate cancer is one of the leading causes of cancer-related death in U.S. men. There is an unmet need to identify modifiable risk factors for prostate cancer survival. Experimental studies have suggested that nonsteroidal anti-inflammatory drugs (NSAIDs) may improve prostate cancer survival through antithrombotic and anti-inflammation mechanisms. Results from previous observational studies have been equivocal, and few have assessed whether an etiologically relevant time window of exposure exists. We sampled incident prostate cancer cases from two large U.S. prospective cohorts, NIH-AARP Diet and Health Study and PLCO Cancer Screening Trial, to investigate whether pre- and postdiagnostic aspirin and non-aspirin NSAID use were associated with prostate cancer-specific and all-cause mortality. Cox proportional hazards regression models estimated hazard ratios (HRs) and 95% confidence intervals (CIs). Study-specific results were meta-analyzed using fixed-effects models. Pre- and postdiagnostic aspirin or non-aspirin NSAID use were not statistically significantly associated with prostate cancer–specific mortality. However, occasional (less than daily) and daily aspirin users five years or more before prostate cancer diagnosis had 18% (HR = 0.82; 95% CI = 0.75–0.90) and 15% (HR = 0.85; 95% CI = 0.77–0.94) reduced all-cause mortality versus nonusers. Similarly, postdiagnostic occasional and daily aspirin use were associated with 17% (HR = 0.83; 95% CI=0.72–0.95) and 25% (HR = 0.75; 95% CI = 0.66–0.86) reduced all-cause mortality, independent of prediagnostic aspirin use. This study suggests that aspirin or non-aspirin NSAIDs are not associated with prostate cancer survival. However, aspirin use both before and after prostate cancer diagnosis was associated with longer overall survival, highlighting the importance of comorbidity prevention among prostate cancer survivors. Cancer Prev Res; 10(7); 410–20. ©2017 AACR.

Study-specific characteristics of prostate cancer cases in the pre-diagnostic NIH-AARP and PLCO cohorts.

Characteristics of prostate cancer cases by status of NSAID use in the past year in the post-diagnostic NIH-AARP and PLCO cohorts.

Four-level frequency of post-diagnostic NSAID use in relation to mortality.

Frequency of pre-diagnostic aspirin and non-aspirin NSAID use in relation to mortality restricted to exclusive users in the past year.

Four-level frequency of pre-diagnostic NSAID use in relation to mortality.

Frequency of pre-diagnostic NSAID use in relation to mortality within the strata of tumor stage (localized vs. regional/distant).

Flow chart showing how pre- and post-diagnostic exposure prostate cancer cohorts were determined from the NIH-AARP and PLCO study populations.

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PDF - 76KB, Supplementary Table 1. Birth weight and height of boys by age of assessment and by birth cohort. Supplementary Table 2. Hazard ratios of prostate cancer in adulthood per 1 kg in birth weight or per 5 cm in height. Supplementary Table 3. Test of proportional hazards assumption by inclusion of a time (age) varying effect of birth weight/childhood height on the risk of prostate cancer, measured as hazard ratio per z-score, in Cox proportional hazards regression models. Supplementary Table 4. Test of proportional hazards assumption by inclusion of a time (age) - birth weight/height z-score cross product term in Cox proportional hazards regression models. Age is divided into quartiles. Supplementary Table 5. Hazard ratios of prostate cancer in adulthood per increase in age-specific height z-score restricted to those with birth weight measures, unadjusted and adjusted for birth weight.

Background: The etiology of male breast cancer is poorly understood, partly due to its relative rarity. Although tobacco and alcohol exposures are known carcinogens, their association with male breast cancer risk remains ill-defined.Methods: The Male Breast Cancer Pooling Project consortium provided 2,378 cases and 51,959 controls for analysis from 10 case–control and 10 cohort studies. Individual participant data were harmonized and pooled. Unconditional logistic regression was used to estimate study design–specific (case–control/cohort) ORs and 95% confidence intervals (CI), which were then combined using fixed-effects meta-analysis.Results: Cigarette smoking status, smoking pack-years, duration, intensity, and age at initiation were not associated with male breast cancer risk. Relations with cigar and pipe smoking, tobacco chewing, and snuff use were also null. Recent alcohol consumption and average grams of alcohol consumed per day were also not associated with risk; only one subanalysis of very high recent alcohol consumption (>60 g/day) was tentatively associated with male breast cancer (ORunexposed referent = 1.29; 95% CI, 0.97–1.71; OR>0– = 1.36; 95% CI, 1.04–1.77). Specific alcoholic beverage types were not associated with male breast cancer. Relations were not altered when stratified by age or body mass index.Conclusions: In this analysis of the Male Breast Cancer Pooling Project, we found little evidence that tobacco and alcohol exposures were associated with risk of male breast cancer.Impact: Tobacco and alcohol do not appear to be carcinogenic for male breast cancer. Future studies should aim to assess these exposures in relation to subtypes of male breast cancer. Cancer Epidemiol Biomarkers Prev; 24(3); 520–31. ©2014 AACR.

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Supplementary material and methods: supplementary information on data collection, statistical analyses, and presentation of results in the figures.

Supplemental Figures. Supplemental Figure 1. AMH distribution for cases and controls. Supplemental Figure 2. AMH levels in all participants stratified by 5 year age groups.

Supplementary Table 3. Associations between alcohol consumption exposures and male breast cancer risk

Supplementary Table 2 from Serum Pepsinogens and Helicobacter pylori in Relation to the Risk of Esophageal Squamous Cell Carcinoma in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study

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Hazard ratios stratified by potential effect modifiers

Background: Previous research has noted higher cancer mortality rates and lower survival among males than females. However, systematic comparisons of these two metrics by sex have been limited.Methods: We extracted U.S. vital rates and survival data from the Surveillance, Epidemiology and End Results Database for 36 cancers by sex and age for the period 1977 to 2006. We compared sex-specific mortality rates and examined male-to-female mortality rate ratios (MRR). We also extracted case data which included age and date of diagnosis, sex, primary cancer site, tumor stage and grade, survival time, vital status, and cause of death. Relative cancer-specific HRs for death in the 5-year period following diagnosis were estimated with Cox proportional hazards models, adjusted for covariates.Results: For the vast majority of cancers, age-adjusted mortality rates were higher among males than females with the highest male-to-female MRR for lip (5.51), larynx (5.37), hypopharynx (4.47), esophagus (4.08), and urinary bladder (3.36). Cancer-specific survival was, for most cancers, worse for males than females, but such disparities were drastically less than corresponding MRRs [e.g., lip (HR = 0.93), larynx (HR = 1.09), hypopharynx (HR = 0.98), esophagus (HR = 1.05), and urinary bladder (HR = 0.83)].Conclusions: Male-to-female MRRs differed markedly while cancer survival disparities were much less pronounced. This suggests that sex-related cancer disparities are more strongly related to etiology than prognosis.Impact: Future analytic studies should attempt to understand causes of observed sex disparities in cancer. Cancer Epidemiol Biomarkers Prev; 20(8); 1629–37. ©2011 AACR.

Background: The combined action of androgens and estrogens—specifically their balance—may play a role in prostate carcinogenesis, but existing evidence is sparse and inconsistent. We investigated associations between serum sex steroid hormones, including estrogen metabolites, and risk of aggressive prostate cancer.Methods: In a case–control study nested within the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial cohort, we measured serum estrone, estradiol, and 13 estrogen metabolites, in the 2-, 4-, or 16-hydroxylation pathways, using an LC/MS-MS assay. Cases (n = 195) were non-Hispanic white men ages 55 to 70 years when diagnosed with aggressive prostate cancer (stage III or IV and/or Gleason ≥7). Controls (n = 195) were non-Hispanic white men without prostate cancer who were frequency matched to cases by age and year at blood draw, and time since baseline screen. Only men with serum testosterone and sex hormone-binding globulin measured previously were eligible. Logistic regression models were used to estimate ORs and 95% confidence intervals (95% CI).Results: Risk of aggressive prostate cancer was strongly inversely associated with estradiol:testosterone ratio (OR4th quartile vs. 1st = 0.27; 95% CI, 0.12–0.59, Ptrend = 0.003) and positively associated with 2:16α-hydroxyestrone ratio (OR4th quartile vs. 1st = 2.44; 95% CI, 1.34–4.45, Ptrend = 0.001). Individual estrogen metabolites were unrelated to risk.Conclusions: Our findings suggest that sex steroid hormones, specifically the estrogen-androgen balance, may be important in the development of aggressive prostate cancer.Impact: Improved understanding of the hormonal etiology of prostate cancer is critical for prevention and therapeutic interventions. Cancer Epidemiol Biomarkers Prev; 23(11); 2374–82. ©2014 AACR.

Supplementary Table 2: Reproducibility of average tissue hormone assays by zone and overall from a pilot study of 30 men recruited at George Washington University Medical Center that included a total of 171 prostate biopsies.

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Background: Iron is an essential micronutrient that can have carcinogenic effects when at high or low concentrations. Previous studies of iron in relation to gastric cancer have not assessed subtype-specific relationships. We used the prospective Alpha-Tocopherol, Beta-Carotene (ATBC) Cancer Prevention Study to assess whether iron metrics were associated with gastric cardia cancer (GCC) and gastric noncardia cancer (GNCC).Methods: We selected 341 incident gastric cancer cases (86 cardia, 172 noncardia, and 83 nonspecified), accrued during 22 years of follow-up, and 341 individually matched controls. We measured prediagnostic serum iron, ferritin, unsaturated iron binding capacity, and C-reactive protein. Total iron-binding capacity (TIBC) and transferrin saturation were estimated from these metrics. Dietary iron exposures were estimated from a food frequency questionnaire. Multivariable logistic regression was used for analysis.Results: Serum iron metrics were not associated with GCC, except for a potential “n”-shaped relationship with TIBC (global P = 0.038). GNCC was inversely associated with serum ferritin (global P = 0.024), serum iron (global P = 0.060) and, possibly, transferrin saturation. TIBC appeared to share a “u”-shaped relationship with GNCC (global P = 0.033). Dietary iron exposures were not associated with either subsite. Adjustment for Helicobacter pylori and gastric atrophy had little effect on observed associations.Conclusions: We found little evidence for the involvement of iron exposure in the pathogenesis of GCC. GNCC was associated with an iron profile similar to that of iron deficiency.Impact: Our findings indicate that inverse associations between iron metrics and gastric cancer are driven by associations with GNCC. Further elucidation of potential mechanisms is warranted. Cancer Epidemiol Biomarkers Prev; 21(11); 2033–42. ©2012 AACR.

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Supplementary Table 2. Associations between tobacco exposures and male breast cancer risk additionally adjusted for total exposure (pack-years)

Supplementary Figure Legends for Figures S1-S15.

The association between leisure-time physical activity (LTPA) and male breast cancer risk is unclear. In the Male Breast Cancer Pooling Project, with 449 cases and 13,855 matched controls, we used logistic regression with study stratification to generate adjusted ORs and 95% confidence intervals (CI) for LTPA tertiles and male breast cancer risk. Compared with low LTPA, medium and high LTPA were not associated with male breast cancer risk (OR, 1.01; 95% CI, 0.79–1.29; 0.90, 0.69–1.18, respectively). In joint-effects analyses, compared with the referent of high body mass index (BMI; ≥25 kg/m2)/low LTPA, neither medium nor high PA was associated with risk among high BMI men, but normal BMI men (2) with low or medium LTPA were at a nonsignificant ∼16% reduced risk and those with high LTPA were at a 27% reduced risk (OR, 0.73; 95% CI, 0.50–1.07). Physical activity alone may not confer protection against male breast cancer risk. Cancer Epidemiol Biomarkers Prev; 24(12); 1898–901. ©2015 AACR.

Supplementary Table 1. Included countries according to obesity prevalence (proportion of body mass index{greater than or equal to}30kg/m2) quartiles in 2008 by sex. Supplementary Table 2a. Countries by obesity (proportion of body mass index{greater than or equal to}30kg/m2) and smoking (approximated by lung cancer mortality in 2012) tertiles, males. Supplementary Table 2b. Countries by obesity (proportion of body mass index{greater than or equal to}30kg/m2) and smoking (approximated by lung cancer mortality in 2012) tertiles, females. Supplementary Table 3. Age-standardized incidence rate ratios by smoking (approximated by age-standardized lung cancer mortality in 2012) and obesity prevalence (proportion of body mass index{greater than or equal to}30kg/m2) in tertiles (1-3, from lowest to highest), using 1st tertile (lowest level of exposure to both risk factors) as reference. Supplementary Figure 1. Age-standardized incidence rates (ASR) of esophageal and gastric cancers by sex and obesity (proportion of body mass index{greater than or equal to}30kg/m2) quartile, excluding China, Japan and Korea. Supplementary Figure 2. Age-specific incidence rates of esophageal and gastric cancers by sex and obesity (proportion of body mass index{greater than or equal to}30kg/m2) quartile, excluding China, Japan and Korea. Supplementary Figure 3. Male-to-female ratios of esophageal and gastric cancer by age and obesity (proportion of body mass index{greater than or equal to}30kg/m2) quartile, excluding China, Japan and Korea. Supplementary Figure 4. Correlations between obesity prevalence (%) and age-standardized incidence of esophageal and gastric cancers by sex.

Supplementary Table 1. Characteristics of the Studies Included in the Male Breast Cancer Pooling Project

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Supplementary Table 1: Reproducibility of serum and tissue hormone assays used for the main analysis

This file contains Supplementary Tables 1-3. Supplementary Table 1 gives the distribution of prostate cancer cases by subtype included in the pooled Analyses of fruit, vegetable, and mature bean consumption and prostate cancer risk. Supplementary Table 2 gives the results of analyses using all main exposures modeled continuously. Supplementary Table 3 provides information on funding information for all cohort studies included in the pooled analysis.

Background: Helicobacter pylori can induce gastric atrophy in humans, which in turn increases gastric cancer risk. Whether H. pylori and gastric atrophy also affect the risk of esophageal squamous cell carcinoma (ESCC), however, remains unresolved.Methods: We performed a nested case-control study within the prospective Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study to assess these relationships. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study is composed of 29,133 Finnish male smokers, ages 50 to 69 years, who were recruited during 1985-1988. Using baseline sera, we assessed H. pylori status (via immunoglobulin G antibodies against whole-cell and CagA antigens) and gastric atrophy status [via the biomarkers pepsinogen I (PGI) and pepsinogen II (PGII)] in 79 ESCC cases and 94 controls. Logistic regression with adjustment for age, date of blood draw, education, cigarette smoking, alcohol, body mass index, and fruit and vegetable intake was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI).Results: Gastric atrophy (PGI/PGII H. pylori and ESCC (OR, 0.94; 95% CI, 0.40-2.24).Conclusions: These results could be explained by misclassification of H. pylori status due to serologic amnesia, ESCC risk being dependent on the functional consequences or interactions of H. pylori rather than the infection per se, gastric atrophy having a different histogenesis in ESCC without being primarily dependent on H. pylori acquisition, or a lack of statistical power to detect an effect.Impact: Validation of these results may warrant mechanistic studies to determine the route of association between gastric atrophy and ESCC. Cancer Epidemiol Biomarkers Prev; 19(8); 1966–75. ©2010 AACR.

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Supplemental Tables. Supplemental Table 1. Baseline characteristics by AMH quartiles. Supplemental Table 2. Baseline characteristics by AMH quartiles restricted to controls only. Supplemental Table 3. Spearmen correlations between circulating AMH levels and androgens in overall and control men with androgen measurements. Supplemental Table 4. Sensitivity analysis: Age-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for AMH quartiles and prostate cancer risk sequentially excluding prostate cancer cases who were diagnosed within two, three and then five years after sera collection. Supplemental Table 5: Sensitivity analyses: Age-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for AMH quartiles and prostate cancer risk. Supplemental Table 6. Sensitivity analysis: Age-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for AMH quartiles and prostate cancer risk restricted to subpopulation with PSA at T0

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Background: Adult height has been positively associated with prostate cancer risk. However, the exposure window of importance is currently unknown and assessments of height during earlier growth periods are scarce. In addition, the association between birth weight and prostate cancer remains undetermined. We assessed these relationships in a cohort of the Copenhagen School Health Records Register (CSHRR).Methods: The CSHRR comprises 372,636 school children. For boys born between the 1930s and 1969, birth weight and annual childhood heights—measured between ages 7 and 13 years—were analyzed in relation to prostate cancer risk. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CI).Results: There were 125,211 males for analysis, 2,987 of who were subsequently diagnosed with prostate cancer during 2.57 million person-years of follow-up. Height z-score was significantly associated with prostate cancer risk at all ages (HRs, 1.13 to 1.14). Height at age 13 years was more important than height change (P = 0.024) and height at age 7 years (P = 0.024), when estimates from mutually adjusted models were compared. Adjustment of birth weight did not alter the estimates. Birth weight was not associated with prostate cancer risk.Conclusions: The association between childhood height and prostate cancer risk was driven by height at age 13 years.Impact: Our findings implicate late childhood, adolescence, and adulthood growth periods as containing the exposure window(s) of interest that underlies the association between height and prostate cancer. The causal factor may not be singular given the complexity of both human growth and carcinogenesis. Cancer Epidemiol Biomarkers Prev; 22(12); 2232–40. ©2013 AACR.

The role of insulin-like growth factors (IGF) in prostate cancer development is not fully understood. To investigate the association between circulating concentrations of IGFs (IGF-I, IGF-II, IGFBP-1, IGFBP-2, and IGFBP-3) and prostate cancer risk, we pooled individual participant data from 17 prospective and two cross-sectional studies, including up to 10,554 prostate cancer cases and 13,618 control participants. Conditional logistic regression was used to estimate the ORs for prostate cancer based on the study-specific fifth of each analyte. Overall, IGF-I, IGF-II, IGFBP-2, and IGFBP-3 concentrations were positively associated with prostate cancer risk (Ptrend all ≤ 0.005), and IGFBP-1 was inversely associated weakly with risk (Ptrend = 0.05). However, heterogeneity between the prospective and cross-sectional studies was evident (Pheterogeneity = 0.03), unless the analyses were restricted to prospective studies (with the exception of IGF-II, Pheterogeneity = 0.02). For prospective studies, the OR for men in the highest versus the lowest fifth of each analyte was 1.29 (95% confidence interval, 1.16–1.43) for IGF-I, 0.81 (0.68–0.96) for IGFBP-1, and 1.25 (1.12–1.40) for IGFBP-3. These associations did not differ significantly by time-to-diagnosis or tumor stage or grade. After mutual adjustment for each of the other analytes, only IGF-I remained associated with risk. Our collaborative study represents the largest pooled analysis of the relationship between prostate cancer risk and circulating concentrations of IGF-I, providing strong evidence that IGF-I is highly likely to be involved in prostate cancer development. Cancer Res; 76(8); 2288–300. ©2016 AACR.

Despite considerable research, the pathogenesis of prostate cancer remains poorly understood. Meanwhile, PSA testing has shifted prostate cancer case populations for study to include a greater proportion of asymptomatic and indolent disease. Thus, efforts to identify prostate cancer biomarkers—particularly for aggressive disease—are required to elucidate pathogenesis and aid screening efficacy. Current evidence suggests that decreased circulating concentrations of the testis-derived, TGFβ family peptide hormone—anti-Müllerian hormone (AMH)—may be associated with prostate cancer pathogenesis. To test this hypothesis, we measured AMH concentrations in prediagnostic (cohort baseline) sera using the Beckman Coulter AMH Gen II ELISA in 1,000 cases and 1,000 controls nested within the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Controls were frequency matched to cases on age at entry, enrollment year, and years of follow-up. Unconditional logistic regression models, adjusted for age at randomization, were used to estimate odds ratios (ORs) and 95% confidence intervals (95% CI). We found that prediagnostic serologic AMH concentrations were not significantly associated with total (ORQ4 vs. Q1 = 1.15; 95% CI, 0.89–1.48; Ptrend = 0.13), aggressive (ORQ4 vs. Q1 = 1.14; 95% CI, 0.80–1.63; Ptrend = 0.51), or nonaggressive (ORQ4 vs. Q1 = 1.22; 95% CI, 0.91–1.63; Ptrend = 0.07) prostate cancer risks. Different definitions of aggressive disease did not meaningfully alter these results. Despite in vitro studies linking AMH to prostate cancer, this first analysis of prediagnostic, circulating AMH concentrations in men provides no evidence for an association with prostate cancer risk. Cancer Epidemiol Biomarkers Prev; 23(11); 2597–602. ©2014 AACR.

Supplemental Table 1: Patient clinical and demographic characteristics. Supplemental Table 2: miRNAs differentially detected among esophageal adenocarcinoma and Barrett's esophagus. Supplemental Table 3: miRNAs differentially expressed among esophageal adenocarcinoma and Barrett's esophagus. Supplemental Table 4: miRNAs differentially expressed among esophageal adenocarcinoma and Barrett's esophagus. Supplemental Table 5: miRNAs differentially detected among early-stage (T1b & T2) esophageal adenocarcinoma and Barrett's esophagus. Supplemental Table 6: miRNAs differentially expressed among early-stage esophageal adenocarcinoma (T1b & T2) and Barrett's esophagus. Supplemental Table 7. Areas Under Receiver Operating Characteristic Curves of Pairwise miR Models Using Five-Fold Cross-Validation. Supplemental Table 8: Summary of published associations between significant top miRNAs and cancer.

Background: The tissue specificity and robustness of miRNAs may aid risk prediction in individuals diagnosed with Barrett's esophagus. As an initial step, we assessed whether miRNAs can positively distinguish esophageal adenocarcinoma from the precursor metaplasia Barrett's esophagus.Methods: In a case–control study of 150 esophageal adenocarcinomas frequency matched to 148 Barrett's esophagus cases, we quantitated expression of 800 human miRNAs in formalin-fixed paraffin-embedded tissue RNA using NanoString miRNA v2. We tested differences in detection by case group using the χ2 test and differences in expression using the Wilcoxon rank-sum test. Bonferroni-corrected statistical significance threshold was set at P < 6.25E−05. Sensitivity and specificity were assessed for the most significant miRNAs using 5-fold cross-validation.Results: We observed 46 distinct miRNAs significantly increased in esophageal adenocarcinoma compared with Barrett's esophagus, 35 of which remained when restricted to T1b and T2 malignancies. Three miRNAs (miR-663b, miR-421, and miR-502-5p) were detected in >80% esophageal adenocarcinoma, but 5-fold increases. Using 5-fold cross-validation, we repeated feature (miR) selection and case–control prediction and computed performance criteria. Each of the five folds selected the same top 10 miRNAs, which, together, provided 98% sensitivity and 95% specificity.Conclusion: This study provides evidence that tissue miRNA profiles can discriminate esophageal adenocarcinoma from Barrett's esophagus. This large analysis has identified miRNAs that merit further investigation in relation to pathogenesis and diagnosis of esophageal adenocarcinoma.Impact: These candidate miRNAs may provide a means for improved risk stratification and more cost-effective surveillance. Cancer Epidemiol Biomarkers Prev; 25(3); 429–37. ©2015 AACR.

PDF file - 92K, Fully adjusted analyses of the association between iron and gastric cancer with cancers diagnosed within 3 years of blood draw excluded

Supplementary Table 3: Multivariable Linear Regressions between Log Continous Serum and Tissue Hormones Stratified by Gleason Score

Risk of aggressive prostate cancer according to cross-classified tertiles of estradiol and testosterone.