Cigarette smoking and prostate cancer recurrence after prostatectomy.

Toward the establishment of evidence-based recommendations for the prevention of prostate cancer recurrence after treatment, we examined the association between smoking and prostate cancer recurrence in a retrospective cohort study of 1416 men who underwent radical prostatectomy. Surgeries were performed by a single surgeon at Johns Hopkins Hospital between January 1, 1993, and March 31, 2006. Smoking status at 5 years before and 1 year after surgery was assessed by survey. Prostate cancer recurrence was defined as confirmed re-elevation of prostate-specific antigen levels, local recurrence, metastasis, or prostate cancer death. The cumulative incidence of recurrence was 34.3% among current smokers, 14.8% among former smokers, and 12.1% among never smokers, with a mean follow-up time of 7.3 years. Men who were current smokers at 1 year after surgery were more likely than never smokers to have disease recurrence after adjusting for pathological characteristics, including stage and grade (hazard ratio for recurrence = 2.31, 95% confidence interval = 1.05 to 5.10). This result suggests an association between cigarette smoking and risk of prostate cancer recurrence.

Association of statin use with pathological tumor characteristics and prostate cancer recurrence after surgery.

PURPOSE: Prospective studies suggest that statins protect against advanced stage and possibly high grade prostate cancer. However, few studies have investigated the influence of stains on outcomes in men with prostate cancer. Thus, we evaluated the association of statin use with pathological tumor characteristics and prostate cancer recurrence after prostatectomy in a retrospective cohort. MATERIALS AND METHODS: A total of 2,399 patients of 1 surgeon at Johns Hopkins Hospital who underwent radical prostatectomy in 1993 to 2006 and had not previously received hormone or radiation therapy were followed for recurrence. The surgeon routinely asked during the preoperative consultation what medications the men were using. Additional information on statin use was obtained from a mailed survey. We estimated the association of statin use with nonorgan confined disease (pT3a/b or N1) and high grade disease (Gleason sum [4 + 3] or greater) using logistic regression (OR), and recurrence using Cox proportional hazards regression (HR). RESULTS: The 16.1% of men who used a statin at prostatectomy were statistically significantly less likely to have nonorgan confined disease than nonusers (OR 0.66, 95% CI 0.50-0.85). Statin use was inversely associated with high grade disease only in men with preoperative PSA 10 ng/ml or greater (OR 0.35, 95% CI 0.13-0.93, p-interaction = 0.02). The HR of recurrence among men who used a statin for 1 year or greater compared to nonusers was 0.77 (95% CI 0.41-1.42). CONCLUSIONS: Our findings support the hypothesis that statin use may protect against prostate cancer with poorer pathological characteristics. We could not rule in or out that longer term statin use may protect against recurrence after prostatectomy.

Reproductive and hormonal factors and the risk of nonsmall cell lung cancer.

Although exposure to estrogen may directly influence or modify the association between cigarette smoking and lung cancer risk, results from epidemiologic studies examining the association between reproductive and hormonal factors and risk of lung cancer among women have been inconsistent. Between 1998 and 2008, 430 women diagnosed with nonsmall cell lung cancer, 316 hospital controls and 295 population controls were recruited into the multi-center Maryland Lung Cancer Study. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) according to reproductive and hormonal exposures adjusting for age, smoking, passive smoking, education and household income. Results were similar for hospital and population based controls, so the control groups were combined. Reduced risks of lung cancer were observed among women with greater parity (≥ 5 vs. 1-2 births: OR = 0.50, 95% CI = 0.32, 0.78, p-trend = 0.002) and later ages at last birth (≥ 30 vs. <25 years old: OR = 0.68, 95% CI = 0.48, 0.98, p-trend = 0.04). After mutual adjustment parity, but not age at last birth, remained significantly inversely associated with risk (p-trend = 0.01). No associations were found for nonsmall cell lung cancer risk with age at menarche, age at first birth, menopausal status, oral contraceptive use or menopausal hormone use, including use of oral estrogens. Compatible with findings from recent epidemiologic studies, we observed a reduction in the risk of nonsmall cell lung cancer with increasing number of births. Other reproductive and hormonal exposures, including menopausal hormone therapy use, were not associated with risk.

Available carbohydrates, glycemic load, and pancreatic cancer: is there a link?

High-carbohydrate diets have been linked to pancreatic cancer risk in case-control studies, but prospective studies have shown mostly null results. The authors investigated the associations of glycemic load, glycemic index, and carbohydrate intake with pancreatic cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Dietary intake was assessed by using a self-administered questionnaire. Between 1998 and 2006 (median follow-up = 6.5 years), 266 incident, confirmed pancreatic cancers were identified among 109,175 participants. Hazards ratios and 95% confidence intervals were adjusted for sex, smoking, body mass index, and total energy. Overall, elevated risks for pancreatic cancer were observed in the 90th versus 10th percentile of glycemic load (hazards ratio (HR) = 1.45, 95% confidence interval (CI): 1.05, 2.00), available carbohydrate (HR = 1.47, 95% CI: 1.05, 2.06), and sucrose (HR = 1.37, 95% CI: 0.99, 1.89) intake. The positive association for available carbohydrate intake was observed during the first 4 years of follow-up (HR(<2 years) = 2.60, 95% CI: 1.34, 5.06; HR(2-<4 years) = 1.94, 95% CI: 1.06, 3.55) but not subsequently (HR = 0.86, 95% CI: 0.52, 1.44); the opposite pattern was observed for total fat and saturated fat intake. Rather than being causal, the short-term increase in pancreatic cancer risk associated with high available carbohydrate and low fat intake may be capturing dietary changes associated with subclinical disease.

Body mass index, effect modifiers, and risk of pancreatic cancer: a pooled study of seven prospective cohorts.

OBJECTIVE: To investigate whether the positive association of body mass index (BMI, kg/m(2)) with risk of pancreatic cancer is modified by age, sex, smoking status, physical activity, and history of diabetes. METHODS: In a pooled analysis of primary data of seven prospective cohorts including 458,070 men and 485,689 women, we identified 2,454 patients with incident pancreatic cancer during an average 6.9 years of follow-up. Cox proportional hazard regression models were used in data analysis. RESULTS: In a random-effects meta-analysis, for every 5 kg/m(2) increment in BMI, the summary relative risk (RR) was 1.06 (95% confidence interval (CI) 0.99-1.13) for men and 1.12 (95% CI 1.05-1.19) for women. The aggregate analysis showed that compared with normal weight (BMI: 18.5 to <25), the adjusted RR was 1.13 (95% CI 1.03-1.23) for overweight (BMI: 25 to <30) and 1.19 (95% CI 1.05-1.35) for obesity class I (BMI: 30 to <35). Tests of interactions of BMI effects by other risk factors were not statistically significant. Every 5 kg/m(2) increment in BMI was associated with an increased risk of pancreatic cancer among never and former smokers, but not among current smokers (P-interaction = 0.08). CONCLUSION: The present evidence suggests that a high BMI is an independent risk factor of pancreatic cancer.

Nonradiation risk factors for thyroid cancer in the US Radiologic Technologists Study.

The incidence of thyroid cancer has been rapidly increasing in the United States, but few risk factors have been established. The authors prospectively examined the associations of self-reported medical history, anthropometric factors, and behavioral factors with thyroid cancer risk among 90,713 US radiologic technologists (69,506 women and 21,207 men) followed from 1983 through 2006. Incident thyroid cancers in 242 women and 40 men were reported. Elevated risks were observed for women with benign thyroid conditions (hazard ratio (HR) = 2.35, 95% confidence interval (CI): 1.73, 3.20), benign breast disease (HR = 1.56, 95% CI: 1.08, 2.26), asthma (HR = 1.68, 95% CI: 1.00, 2.83), and body mass index > or =35.0 versus 18.5-24.9 kg/m(2) (HR = 1.74, 95% CI: 1.03, 2.94; P-trend = 0.04). Current smoking was inversely associated with thyroid cancer risk (HR = 0.54). No clear associations emerged for reproductive factors, other medical conditions, alcohol intake, or physical activity. Despite few thyroid cancers in men, men with benign thyroid conditions had a significantly increased risk of thyroid cancer (HR = 4.65, 95% CI: 1.62, 13.34), and results for other risk factors were similar to those for women. Consistent with prior studies, obesity and benign thyroid conditions increased and current smoking decreased the risk of thyroid cancer. The novel findings for benign breast disease and asthma warrant further investigation.

Folate intake, post-folic acid grain fortification, and pancreatic cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.

BACKGROUND: Folate plays a critical role in DNA methylation, synthesis, and repair. Several epidemiologic studies suggest that higher folate intake is associated with decreased pancreatic cancer risk. OBJECTIVE: We investigated the association between dietary folate intake and pancreatic cancer in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) cohort. DESIGN: Dietary data were collected with the use of a self-administered food-frequency questionnaire (1998-2005). Among the 51,988 male and 57,187 female participants, aged 55-74 y at enrollment, with complete dietary and multivitamin information, 162 men and 104 women developed pancreatic cancer during follow-up (January 1998 to December 2006; median: 6.5 y). We used Cox proportional hazards regression with age as the time metric to calculate hazard ratios (HRs) and 95% CIs. RESULTS: The highest compared with the lowest quartile of food folate was associated with a significantly decreased pancreatic cancer risk among women (> or = 253.3 compared with < or = 179.1 microg/d; HR = 0.47; 95% CI: 0.23, 0.94; P for trend: 0.09) but not among men (> or = 229.6 compared with < or = 158.0 microg/d; HR = 1.20; 95% CI: 0.70, 2.04; P for trend: 0.67; P for interaction by sex: 0.03). There was also a significant inverse trend in risk of pancreatic cancer across increasing quartiles of total folate in women (P for trend: 0.04) but not in men (P for trend: 0.65). Folic acid supplements were not associated with pancreatic cancer. CONCLUSION: These findings support an association between higher food and total folate intakes and decreased risk of pancreatic cancer in women but not in men.

Predictors of fasting serum insulin and glucose and the risk of pancreatic cancer in smokers.

OBJECTIVES: A history of type 2 diabetes is one of few consistent risk factors for pancreatic cancer. Potentially modifiable factors related to fasting insulin and glucose concentrations may influence pancreatic cancer risk. METHODS: Multiple linear regression models were used to identify anthropometric, clinical, behavioral, and dietary factors associated with fasting insulin and glucose in a subcohort of non-diabetics in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (n = 366). Hazards ratios (HRs) and 95% confidence intervals (CIs) were calculated among the larger cohort (n = 27,035). RESULTS: During follow-up (median 16.1 years), 305 participants developed pancreatic cancer. Fasting insulin and/or glucose were positively associated with body mass index (BMI), height, and dietary total and saturated fat and inversely associated with serum high-density lipoprotein cholesterol (HDL) and dietary available carbohydrates, sucrose, and alcohol. Comparing highest to lowest quintiles, total fat (HR = 1.54, 95% CI 1.05-2.25, p-trend = 0.01) and saturated fat (HR = 1.38, 95% CI 0.97-1.98, p-trend = 0.06) were positively associated and available carbohydrates (HR = 0.63, 95% CI 0.44-0.90, p-trend = 0.01), particularly sucrose (HR = 0.62, 95% CI 0.43-0.89, p-trend = 0.09), were inversely associated with risk of pancreatic cancer. BMI, HDL, height, and alcohol were not associated with pancreatic cancer risk. CONCLUSION: Dietary fat is associated with higher fasting insulin concentrations and may increase pancreatic cancer risk in smokers.