Studies on the relationship between obesity and prostate cancer incidence are inconsistent. In part, this inconsistency may be due to a differential effect of obesity on low-grade and high-grade cancer or confounding of the association of obesity with prostate cancer risk by diabetes. We investigated the associations of obesity and diabetes with low-grade and highgrade prostate cancer risk.

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BACKGROUNDCurrent research is inconclusive regarding the effect of obesity on outcomes after a prostate cancer diagnosis. The objective of this study was to examine associations between obesity and the risks of developing metastasis or prostate cancer‐specific mortality in a population‐based cohort of men with prostate cancer.METHODSSeven hundred fifty‐two middle‐aged men with prostate cancer who were enrolled in a case‐control study and remain under long‐term follow‐up for disease progression and mortality formed the study cohort. Body mass index (BMI) in the year before diagnosis was obtained at the time of initial interview. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) of prostate cancer metastasis and mortality associated with obesity, controlling for age, race, smoking status, Gleason score, stage at diagnosis, diagnostic prostate‐specific antigen level, and primary treatment.RESULTSObesity (BMI ≥30 kg/m2) was associated with a significant increase in prostate cancer mortality (HR, 2.64; 95% CI, 1.18–5.92). Among men who were diagnosed with local‐ or regional‐stage disease, obesity also was associated with an increased risk of developing metastasis (HR, 3.61; 95% CI, 1.73–7.51). Associations generally were consistent across strata defined by Gleason score (2–6 or 7 [3 + 4] vs 7 [4 + 3] or 8–10), stage (local vs regional/distant for mortality), and primary treatment (androgen‐deprivation therapy use: yes vs no).CONCLUSIONSObesity at the time of diagnosis was associated with increased risks of prostate cancer metastasis and death. The increased risk of prostate cancer death or metastasis associated with obesity largely was independent of key clinical prognostic factors at diagnosis. Cancer 2007. © 2007 American Cancer Society.

Smoking at the time of diagnosis, independent of key clinical prognostic factors, is associated with an increased risk of prostate cancer death.

BackgroundObesity has been shown to be inversely associated with breast cancer risk in premenopausal women, while increasing risk in postmenopausal women. However, the current evidence is largely based on studies in Caucasian populations. Associations in women of African ancestry (AA), who have a higher prevalence of obesity, have been evaluated in few studies and results suggest different effects.MethodsWe evaluated the impact of body size, body fat distribution, and body composition on breast cancer risk among AA women (978 cases and 958 controls) participating in the Women’s Circle of Health Study, a multi-site case–control study in New York City (NYC) and New Jersey (NJ). Cases were newly diagnosed with histologically confirmed ductal carcinoma in situ or invasive breast cancer, age 20–75 yrs. In NYC, cases were recruited through hospitals with the largest referral patterns for AA women and controls through random digit dialing (RDD). In NJ, cases were identified in seven counties in NJ thorough the NJ State Cancer Registry, and controls through RDD and community-based recruitment. During in-person interviews, questionnaires were administered and detailed anthropometric measurements were obtained. Body composition was assessed by bioelectrical impedance analysis.ResultsBMI did not have a major impact on pre- or post-menopausal breast cancer, but was significantly associated with reduced risk of ER-/PR- tumors among postmenopausal women (OR: 0.37; 95% CI: 0.15-0.96 for BMI > 30 vs. BMI < 25). Furthermore, increased premenopausal breast cancer risk was found for higher waist and hip circumferences after adjusting for BMI, with ORs of 2.25 (95% CI: 1.07-4.74) and 2.91 (95% CI: 1.39-6.10), respectively, comparing the highest vs. lowest quartile. While ORs for higher fat mass and percent body fat among postmenopausal women were above one, confidence intervals included the null value.ConclusionsOur study suggests that in AA women BMI is generally unrelated to breast cancer. However, higher waist and hip circumferences were associated with increased pre-menopausal breast cancer risk, while general obesity was associated with decreased risk of ER-/PR- tumors. Larger studies are needed to confirm findings and to evaluate the impact of obesity on breast cancer subtypes.

Immune signatures in breast tumors differ by estrogen receptor (ER) status. The purpose of this study was to assess associations between ER phenotypes and circulating levels of cytokines that co-ordinate cell-mediated [T-helper type 1 (Th1)] and humoral [T-helper type 2 (Th2)] immunity. We conducted a case–case comparison of 523 women with newly diagnosed breast cancer to evaluate associations between 27 circulating cytokines, measured using Luminex XMap technology, and breast cancer phenotypes [ER− vs. ER+; triple negative breast cancer (TNBC) vs. luminal A (LumA)]. Ratios of Th1 to Th2 cytokines were also evaluated. Levels of interleukin (IL)-5, a Th-2 cytokine, were higher in ER− than in ER+ tumors. The highest tertile of IL-5 was more strongly associated with ER− (OR = 2.33, 95 % CI 1.40–3.90) and TNBCs (OR = 2.78, 95 % CI 1.53–5.06) compared to ER+ and LumA cancers, respectively, particularly among premenopausal women (OR = 4.17, 95 % CI 1.86–9.34, ER− vs. ER+; OR = 5.60, 95 % CI 2.09–15.01, TNBC vs. LumA). Elevated Th1 cytokines were also detected in women with ER− and TNBCs, with women in the highest tertile of interferon α2 (OR = 2.39, 95 % CI 1.31–4.35) or tumor necrosis factor-α (OR = 2.27, 95 % CI 1.21–4.26) being twice as likely to have TNBC versus LumA cancer. When cytokine ratios were examined, women with the highest ratios of Th1 cytokines to IL-5 levels were least likely to have ER− or TNBCs compared to ER+ or LumA cancers, respectively. The strongest associations were in premenopausal women, who were up to 80 % less likely to have TNBC than LumA cancers (IL-12p40/IL-5, OR = 0.19, 95 % CI 0.07–0.56). These findings indicate that immune function is associated with ER− and TNBC and may be most relevant among younger women, who are likely to be diagnosed with these aggressive phenotypes.

Objective Folate and other methyl-group nutrients may play a key role in pancreatic carcinogenesis through their effects on DNA integrity. We examined the association between pancreatic cancer and intake of folate, vitamins B6, B12 and methionine in a large population-based case-control study. Methods Risk factor data were collected during in-person interviews with 532 pancreatic cancer cases diagnosed in 1995-1999 and 1701 frequency-matched controls in the San Francisco Bay Area. Dietary history and supplement use were obtained using a semi-quantitative food frequency questionnaire developed at Harvard University. Adjusted unconditional logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (CI) as estimates of the relative risk. Results Total folate intake was inversely associated with pancreatic cancer (5th vs. 1st quintile: OR=0.67, 95% CI=0.48-0.93, Ptrend=0.04). Increased vitamin B12 from food was positively associated with pancreatic cancer although risk estimates for quintiles 3 to 5 were similar (5th vs. 1st quintile: OR=1.9, 95% CI=1.3-2.6, Ptrend=0.001). Intake of vitamin B6 or methionine was not associated with pancreatic cancer risk. Conclusions Our study provided some support for an inverse association between folate intake and pancreatic cancer risk. The increased pancreatic cancer risk with vitamin B12 intake from food warrants further investigation.

Patient vital status generally is passively obtained by cancer registries, and no previous population-based studies have used extensive active follow-up to compute a more accurate overall survival rate for pancreatic cancer. Therefore, the authors used multiple active and passive follow-up methods to determine vital status and date of death for 1,954 pancreatic cancer patients diagnosed from 1995 to 1999 in a large population-based study in the San Francisco Bay Area, California. Survival rates were estimated by using Kaplan-Meier methods. Hazard ratios and 95% confidence intervals were estimated by using multivariable Cox proportional-hazards models. Vital status was confirmed for >99% of 1,954 patients. The overall 5-year survival rate was 1.3% and was greater in patients who were younger and who had localized disease, well-differentiated tumors, and surgical resection. Shorter survival was associated with older age at diagnosis, male sex, distant/metastatic disease, and poorly differentiated tumors. Longer survival was observed for Asian/Pacific Islanders compared with non-Hispanic whites and for any active treatment regardless of tumor stage. With an almost complete follow-up, the authors observed a low overall 5-year survival rate. Although the results provide further evidence of poor survival among patients with pancreatic cancer, the data also suggest that within-stage-of-disease patients survived somewhat longer with therapy.