Risk Of Fatal Cancer Research Articles

Abstract 3009: Lipid-lowering drug use and risk of fatal prostate cancer in the Atherosclerosis Risk in Communities (ARIC) Study

Abstract Background: Studies show that lipid-lowering medications, particularly statins, may be protective for more aggressive prostate cancer. Lethal prostate cancer is often considered an optimal outcome in epidemiologic studies when the aim is to identify modifiable risk factors with the potential to reduce morbidity and mortality from this disease, yet this outcome remains understudied. Further, lipid drug use and prostate cancer risk is understudied in black men, whose risk of fatal prostate cancer is 2-3 times higher than that of white men. Thus, we studied lipid medication use and fatal prostate cancer risk in the ARIC Study, which includes ~25% black participants. Methods: The ARIC Study is a prospective cohort that included 15,792 participants (7,082 men) recruited from four US communities. We conducted a prospective cohort analysis of 6,547 men who attended visit 2 (1990-1992, the start of the statin era) and were followed for cancer death through 12/31/2012. Death from prostate cancer (n=90) as the underlying cause was obtained from death certificates supplemented with medical records. Updated information on medication use was collected throughout the study follow-up during study visits and annual telephone calls. Lipid medication use was modeled as a time-dependent variable in two ways: 1) current use (yes/no), and 2) duration of use (<10, ≥10 years). Cox proportional hazards regression was used to estimate the hazard ratio (HR) and 95% confidence interval (CI) of prostate cancer death overall and by race. All models were adjusted for age (years), race, and study center. Additional models were further adjusted for height, BMI, smoking, diabetes, and education. Results: The prevalence of lipid medication use was 17% by visit 4, partway into the statin drug era, and 76% of those medications were statins. After adjustment for age, race, and study center, men who used lipid medications were statistically significantly less likely to die from prostate cancer than men who did not use lipid medications (HR=0.56, 95% CI=0.33-0.95). This finding was slightly attenuated after further mutlivariable adjustment (HR=0.62, 0.36-1.08). The statistically significant inverse association appeared to be restricted to men who used lipid medications for ≥10 years (vs. never use: HR=0.39, 95% CI=0.19-0.82, p-trend=0.02). Lipid medication use was inversely associated with a reduced risk of prostate cancer death in both white and black men. Conclusions: Use of lipid medications was associated with a lower risk of fatal prostate cancer in both black and white men. Whether the fact that black men are less likely to receive/take lipid medications could partly explain the black-white disparity in prostate cancer in the US requires further study. Support: NHLBI contracts, NCI grant, NPCR Citation Format: Alison M. Mondul, Corinne E. Joshu, John Barber, Anna Prizment, Nrupen Bahvsar, Josef Coresh, Elizabeth Selvin, Aaron Folsom, Elizabeth A. Platz. Lipid-lowering drug use and risk of fatal prostate cancer in the Atherosclerosis Risk in Communities (ARIC) Study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3009. doi:10.1158/1538-7445.AM2017-3009

Abstract 2306: Sleep duration and risk of fatal prostate cancer in CPS-I and CPS-II

Abstract There is growing evidence that factors associated with circadian rhythm disruption may be associated with prostate cancer risk. In a previous analysis focusing on shift-work in the Cancer Prevention Study (CPS)-II that included only employed men, we observed an association between short sleep duration and higher risk of prostate cancer death that was limited to the first eight years of follow-up of the cohort. To corroborate and expand on these results, we examined the association between sleep duration and death from prostate cancer in a combined analysis of men in CPS-II and men enrolled in an earlier cohort study, CPS-I, regardless of employment status. After excluding men with uninterpretable sleep information, prevalent cancer and prevalent prostate disease at baseline, the analysis included 407,649 men from CPS-I followed from 1950 through 1972, and 416,040 men from CPS-II followed from 1982 through 2012. During follow-up, 1,546 men in CPS-I and 8,704 men in CPS-II died of prostate cancer. Cox proportional hazards regression was used to estimate multivariable-adjusted relative risks (RR) and 95% confidence intervals (CI) and estimates were meta-analyzed using a fixed-effects model because the design and population of CPS-I and CPS-II were similar. Among men aged 65 years and younger, short sleep duration was associated with higher risk of death from prostate cancer during the first eight years of follow-up; compared to 7 hours/night, the RRs (95% CIs) for 3-5, and 6 hours/night were 1.61 (1.10-2.37), and 1.25 (0.99-1.58), respectively. Among men older than age 65 years, the corresponding RRs (95% CIs) were 0.97 (0.68, 1.38), and 1.02 (0.82, 1.27), respectively. There was no association between sleep duration and fatal prostate cancer during later follow-up. These findings support evidence that factors related to circadian rhythms may increase fatal prostate cancer risk. The observed association between short sleep duration and higher risk of fatal prostate cancer only during the first 8-years of follow-up suggests that short sleep duration could affect later stages of prostate carcinogenesis. Reasons for lack of an association in older men are unclear but may include the marked decline in nocturnal melatonin levels with age, which could reduce the relative biologic impact of melatonin inhibition by sleep-deprivation. Citation Format: Susan M. Gapstur, Victoria L. Stevens, Brian D. Carter, Ying Wang, Eric J. Jacobs. Sleep duration and risk of fatal prostate cancer in CPS-I and CPS-II [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2306. doi:10.1158/1538-7445.AM2017-2306

Weight change, obesity and risk of prostate cancer progression among men with clinically localized prostate cancer.

Obesity is associated with an increased risk of fatal prostate cancer. We aimed to elucidate the importance and relevant timing of obesity and weight change for prostate cancer progression. We identified 5,158 men diagnosed with localized prostate cancer (clinical stage T1/T2) from 1986 to 2012 in the Health Professionals Follow-up Study. Men were followed for biochemical recurrence and lethal prostate cancer (development of distant metastasis or prostate cancer-specific mortality) until 2012. Cox regression estimated hazard ratios (HRs) for body mass index (BMI) at age 21, BMI at diagnosis, "long-term" weight change from age 21 to diagnosis and "short-term" weight change over spans of 4 and 8 years preceding diagnosis. Because weight, weight change and mortality are strongly associated with smoking, we repeated analyses among never smokers only (N = 2,559). Among all patients, neither weight change nor BMI (at age 21 or at diagnosis) was associated with lethal prostate cancer. Among never smokers, long-term weight gain was associated with an increased risk of lethal disease (HR for gaining >30 pounds vs. stable weight [±10 pounds] 1.59, 95% CI, 1.01-2.50, p-trend = 0.06). Associations between weight change, BMI and lethal prostate cancer were stronger for men with BMI ≥ 25 at age 21 compared to those with BMI < 25. Weight change and obesity were not associated with an increased risk of biochemical recurrence. Our findings among never smoker men diagnosed with localized prostate cancer suggest a positive association between long-term weight gain and risk of lethal prostate cancer. Metabolic changes associated with weight gain may promote prostate cancer progression.

24O - Increased long-term risk of fatal breast cancer in patients with high intra-tumor heterogeneity of the estrogen receptor – Retrospective analyses of the STO-3 trial

24O - Increased long-term risk of fatal breast cancer in patients with high intra-tumor heterogeneity of the estrogen receptor – Retrospective analyses of the STO-3 trial

Predictions of space radiation fatality risk for exploration missions

In this paper we describe revisions to the NASA Space Cancer Risk (NSCR) model focusing on updates to probability distribution functions (PDF) representing the uncertainties in the radiation quality factor (QF) model parameters and the dose and dose-rate reduction effectiveness factor (DDREF). We integrate recent heavy ion data on liver, colorectal, intestinal, lung, and Harderian gland tumors with other data from fission neutron experiments into the model analysis. In an earlier work we introduced distinct QFs for leukemia and solid cancer risk predictions, and here we consider liver cancer risks separately because of the higher RBE's reported in mouse experiments compared to other tumors types, and distinct risk factors for liver cancer for astronauts compared to the U.S. population. The revised model is used to make predictions of fatal cancer and circulatory disease risks for 1-year deep space and International Space Station (ISS) missions, and a 940 day Mars mission. We analyzed the contribution of the various model parameter uncertainties to the overall uncertainty, which shows that the uncertainties in relative biological effectiveness (RBE) factors at high LET due to statistical uncertainties and differences across tissue types and mouse strains are the dominant uncertainty. NASA's exposure limits are approached or exceeded for each mission scenario considered. Two main conclusions are made: 1) Reducing the current estimate of about a 3-fold uncertainty to a 2-fold or lower uncertainty will require much more expansive animal carcinogenesis studies in order to reduce statistical uncertainties and understand tissue, sex and genetic variations. 2) Alternative model assumptions such as non-targeted effects, increased tumor lethality and decreased latency at high LET, and non-cancer mortality risks from circulatory diseases could significantly increase risk estimates to several times higher than the NASA limits.

Characterization of Environmental Radioactivity Level in Al-Basrah City (Iraq)

Soils and earth-derived building materials contain radioactive materials provide external exposure to nearby individuals and result in detrimental health effects including cancer. The risk of cancer incidence (morbidity) and mortality to individuals in Al-Basrah’s population (south of Iraq) related to external exposure to ambient gamma radiation is evaluated in this study. The risk estimations include delayed radiation effects (cancer morbidity, mortality and hereditary genetic damages). Radiation exposure rates were measured using BGS-4 gamma-ray scintillation (Scintrex, Canada) for the period 2012-2013. Absorbed dose rates in air and in human tissues are determined by applying typical conversion factors available in the literature. Age-dependent radiation dose is calculated for infants, children, and adults. Dose-to-risk conversion factors are applied to estimate potential risk to various body organs and tissues as a result of exposure to ambient gamma radiation. The findings of this study report that about 0.26% of Al-Basrah population are expected to be diagnosed with radiation-induced cancer over there lifetime. The lifetime fatal cancer probability (mortality) is found to be occurs at a rate of 0.19%. The risk of developing fatal stomach cancer is found to be occurs at a largest extent in comparison with other exposed body organs and tissues. Children and infants are found to be at a greater radiation risk than adults due to lower body weight. Other consequences of radiation injury such as genetic effects transmitted to succeeding generations are expected to occur at a rate of 0.03% in the offspring of Al-Basrah population as a result of changes transmitted via the genetic mechanisms due to irradiation of gonads.

Prediagnostic Body Mass Index Trajectories in Relation to Prostate Cancer Incidence and Mortality in the PLCO Cancer Screening Trial.

Evidence suggests that obesity in adulthood is associated with increased risk of "clinically significant" prostate cancer. However, studies of body mass index (BMI) across the adult life course and prostate cancer risks remain limited. In a prospective cohort of 69 873 men in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, we examined associations of prediagnostic BMI across the adult life course with risk of incident prostate cancer and fatal prostate cancer (prostate cancer-specific mortality). At 13 years of follow-up, we identified 7822 incident prostate cancer cases, of which 3078 were aggressive and 255 fatal. BMI trajectories were determined using latent-class trajectory modeling. Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). BMI at age 20 years, 50 years, and baseline questionnaire (mean age = 63 years) were associated with increased risks of fatal prostate cancer (HRs = 1.27-1.32 per five-unit increase). In five BMI trajectories identified, fatal prostate cancer risk was increased in men who had a normal BMI (HR = 1.95, 95% CI = 1.21 to 3.12) or who were overweight (HR = 2.65, 95% CI = 1.35 to 5.18) at age 20 years and developed obesity by baseline compared with men who maintained a normal BMI. Aggressive and nonaggressive prostate cancer were not associated with BMI, and modest inverse associations were seen for total prostate cancer. Our results suggest that BMI trajectories during adulthood that result in obesity lead to an elevated risk of fatal prostate cancer.

Metformin for Reducing Racial/Ethnic Difference in Prostate Cancer Incidence for Men with Type II Diabetes.

Racial/ethnic disparity in prostate cancer is under studied in men with diabetes who are at a higher risk of aggressive prostate cancer. This study assessed the race/ethnic disparity in prostate cancer incidence for men with type II diabetes (T2D) and whether the impact of metformin on prostate cancer incidence varied by race/ethnicity. We conducted a retrospective study in 76,733 male veterans with T2D during 2003 to 2012. Cox proportional hazards model adjusting for covariates and propensity scores of metformin use and race/ethnic group membership was utilized to compute the HR of prostate cancer incidence associated with race/ethnicity and compare HR associated with metformin use between race/ethnic groups. Mean follow-up was 6.4 ± 2.8 years; 7% were Hispanics; 17% were African Americans (AA); mean age was 67.8 ± 9.8 years; 5.2% developed prostate cancer; and 38.9% used metformin. Among these diabetic men without metformin use, prostate cancer incidence was higher in Hispanics and AA than in non-Hispanic White (NHW). Use of metformin alone or metformin + statins was associated with a greater prostate cancer incidence reduction in Hispanics compared with NHW, but not between AA and NHW. Use of metformin + finasteride was associated with a greater prostate cancer incidence reduction in Hispanics and AA compared with NHW. Our results suggested that metformin treatment could be a potential strategy to reduce prostate cancer incidence in the minority populations who are at high risk for fatal prostate cancer. It will be important to further examine the pleiotropic effects of metformin in multi-race/ethnic prospective studies to better inform clinical management and potentially reduce racial/ethnic disparity in prostate cancer incidence among diabetic men. Cancer Prev Res; 9(10); 779-87. ©2016 AACR.

Effect of Extensive Use of Granite Countertops on the γ-Radiation Dose to Occupants of the New Buildings of King Abdulaziz University

Exposure dose due to γ-radiation was measured in the new buildings of King Abdulaziz University using an advanced car-borne monitoring system to evaluate the effect of the extensive use of granites on the exposure dose rate to occupants. The measurements were conducted inside and outside the new buildings. For comparison, measurements inside the old buildings of limited granite use were conducted. The results indicated that the average exposure dose rate in the corridors of granite countertops was 0.115 μSv/h compared to 0.093 μSv/h in corridors of marble floors in the old buildings. About 4.2% increase in the annual effective dose due granite use was estimated. A maximum excess fatal cancer risk to an individual working in the new buildings due to exposure to excess γ-radiation from granite countertops was estimated by 1.4x10-6. The obtained results are discussed in detail and some conclusions are drawn.

Higher BMI, waist circumference associated with increased risk of prostate cancer

Ahigher body mass index (BMI) and waist circumference are associated with an increased risk of aggressive prostate cancer, according to a study of nearly 150,000 men from 8 European countries. This analysis of the European Prospective Investigation Into Cancer and Nutrition (EPIC) was performed by Aurora Pérez-Cornago, PhD, a nutritional epidemiologist in the cancer epidemiology unit at the University of Oxford in England, and her colleagues. They presented their findings at the 2016 European Obesity Summit, which was held June 1–4 in Gothenburg, Sweden. To date, evidence for the association of body size and obesity with prostate cancer risk has been unclear. Dr. Pérez-Cornago and her team investigated the associations between various body measurements at baseline and risk of prostate cancer incidence. They focused on tumor stage and grade as well as mortality. The participants included 141,896 men with a mean age of 52 years from Italy, Spain, the United Kingdom, the Netherlands, Greece, Germany, Sweden, and Denmark. Data were adjusted for education level, smoking, marital status, diabetes, and physical activity. Specifically, investigators focused on high-grade cancers and those that resulted in death. Men with a higher BMI and waist circumference had an increased risk of more aggressive, high-grade prostate cancer (10% increased risk for every 5 kg/m2 increase in BMI and 13% increased risk for every 10-cm increase in waist circumference). Moreover, a 14% higher risk for fatal prostate cancer was observed for every 5 kg/m2 increase in BMI along with an 18% increased risk for every 10 cm of additional waist circumference.

Monte Carlo Simulation of Radiotherapy for Breast Cancer in Pregnant Patients: How to Reduce the Radiation Dose and Risks to Fetus?

This study estimated the fetal dose and risks from radiotherapy for breast cancer with 6 MV X-rays. Breast irradiation was simulated with the MCNP code using two mathematical phantoms corresponding to patients in the early and middle periods of pregnancy. Monte Carlo simulations were performed to determine the appropriate fetal shielding. For a 50-Gy tumor dose, the unshielded fetal dose reached up to 133.1 mGy. Fetal protection with a lead shield of dimensions 30×30×5 cm3 placed besides the treatment couch resulted in maximum doses of 22.0 and 70.3 mGy at the first and second trimesters of gestation, respectively. These shielded fetal doses may be associated with a fatal cancer risk during childhood up to 0.42% and a maximum probability for the appearance of heritable effects of 0.17%. The use of fetal shielding ensures the absence of deterministic effects from radiotherapy during the first 24 weeks of gestation.

Abstract 1755: Weight change, prostate cancer-specific mortality, and biochemical recurrence in a prospective cohort study of U.S. men

Abstract Obesity is associated with an increased risk of fatal prostate cancer. However, the relevant timing of obesity for risk has not been established, and the impact of weight change on prognosis has been understudied. We prospectively investigated the association between weight change and obesity with prostate cancer outcomes among 5,173 men diagnosed with prostate cancer (clinical TNM-stage &amp;lt;T3b) from 1986 to 2012 in the Health Professionals Follow-up Study. Men were followed for biochemical recurrence, development of distant metastasis, and mortality until 2014. Cox proportional hazards models were used to estimate hazard ratios for change in weight from age 21 to diagnosis and in the 4 years prior to diagnosis, adjusting for potential confounding by lifestyle and clinical factors. Because weight, weight change, and mortality are strongly associated with smoking, we conducted the analysis among all prostate cancer patients and among never smokers only (N = 2,554). Among all patients, weight gain from age 21 to the time of diagnosis was associated with risk of lethal prostate cancer (distant metastases or prostate cancer death). Compared to those with stable weight (±10 lbs) from age 21 to diagnosis, those who gained &amp;gt;30 lbs had a 1.44-fold higher risk of lethal cancer (95% CI 1.03-2.01, p-trend = 0.06, adjusting for lifestyle factors, stage, grade, PSA at diagnosis, and weight at age 21). Among never smokers, this association was stronger (HR 2.19, 95% CI 1.31-3.68, p-trend = 0.005). Weight gain in the 4 years preceding diagnosis was suggestively, but not significantly, associated with lethal cancer among never smokers (HR for &amp;gt;5 lbs gain vs stable weight [±5 lbs] 1.48, 95% CI, 0.96, 2.28). No significant associations were found between weight change and biochemical recurrence. Our findings suggest a positive association between adult weight gain and risk of lethal prostate cancer. Metabolic changes associated with weight gain may promote prostate cancer progression. Citation Format: Barbra Dickerman, Thomas Ahearn, Edward Giovannucci, Lorelei Mucci, Kathryn Wilson. Weight change, prostate cancer-specific mortality, and biochemical recurrence in a prospective cohort study of U.S. men. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1755.

Polonium in size fractionated mainstream cigarette smoke, predicted deposition and associated internal radiation dose

In this study, size fractionated mass and 210Po activity concentrations in mainstream cigarette smoke (MCS) were monitored for three popular cigarette brands. Size segregated collection of MCS was carried out using a cascade type impactor, while mass and 210Po activity concentration were analyzed gravimetrically and alpha spectrometry (following the radiochemical separation) respectively. Multiple-Path Particle Dosimetry (MPPD V2.11) model is used for prediction of deposition fraction calculations for the MCS deposition in different compartment of human respiratory tract. The activity concentration of 210Po is founds 10.56 ± 2.46 mBq per cigarette for the tested cigarette brands. 210Po size distribution indicates most of this associates with fine fraction (Dp < 2.23 μm) of cigarette smoke. The committed annual effective dose to smokers (smoking on an average 20 cigarette a day), considering the 210Po and 210Pb concentrations (assuming it is in secular equilibrium with 210Po) in MCS, was estimated between 0.22 and 0.40 mSv, with mean value of 0.30 mSv for tested cigarette brands. Considering the risk factor of fatal cancer due to radiation exposure of lung (exposure time of 30 years); the average collective estimated fatal cancer risk is estimated as 1.5 × 10−4 due to 210Po and 210Pb exposure to smokers.

Body mass index in relation to serum prostate-specific antigen levels and prostate cancer risk.

High Body mass index (BMI) has been directly associated with risk of aggressive or fatal prostate cancer. One possible explanation may be an effect of BMI on serum levels of prostate-specific antigen (PSA). To study the association between BMI and serum PSA as well as prostate cancer risk, a large cohort of men without prostate cancer at baseline was followed prospectively for prostate cancer diagnoses until 2015. Serum PSA and BMI were assessed among 15,827 men at baseline in 2010-2012. During follow-up, 735 men were diagnosed with prostate cancer with 282 (38.4%) classified as high-grade cancers. Multivariable linear regression models and natural cubic linear regression splines were fitted for analyses of BMI and log-PSA. For risk analysis, Cox proportional hazards regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) and natural cubic Cox regression splines producing standardized cancer-free probabilities were fitted. Results showed that baseline Serum PSA decreased by 1.6% (95% CI: -2.1 to -1.1) with every one unit increase in BMI. Statistically significant decreases of 3.7, 11.7 and 32.3% were seen for increasing BMI-categories of 25 < 30, 30 < 35 and ≥35 kg/m(2), respectively, compared to the reference (18.5 < 25 kg/m(2)). No statistically significant associations were seen between BMI and prostate cancer risk although results were indicative of a positive association to incidence rates of high-grade disease and an inverse association to incidence of low-grade disease. However, findings regarding risk are limited by the short follow-up time. In conclusion, BMI was inversely associated to PSA-levels. BMI should be taken into consideration when referring men to a prostate biopsy based on serum PSA-levels.

Associations between unprocessed red and processed meat, poultry, seafood and egg intake and the risk of prostate cancer: A pooled analysis of 15 prospective cohort studies.

Reports relating meat intake to prostate cancer risk are inconsistent. Associations between these dietary factors and prostate cancer were examined in a consortium of 15 cohort studies. During follow-up, 52,683 incident prostate cancer cases, including 4,924 advanced cases, were identified among 842,149 men. Cox proportional hazard models were used to calculate study-specific relative risks (RR) and then pooled using random effects models. Results do not support a substantial effect of total red, unprocessed red and processed meat for all prostate cancer outcomes, except for a modest positive association for tumors identified as advanced stage at diagnosis (advanced(r)). For seafood, no substantial effect was observed for prostate cancer regardless of stage or grade. Poultry intake was inversely associated with risk of advanced and fatal cancers (pooled multivariable RR [MVRR], 95% confidence interval, comparing ≥ 45 vs. <5 g/day: advanced 0.83, 0.70-0.99; trend test p value 0.29), fatal, 0.69, 0.59-0.82, trend test p value 0.16). Participants who ate ≥ 25 versus <5 g/day of eggs (1 egg ∼ 50 g) had a significant 14% increased risk of advanced and fatal cancers (advanced 1.14, 1.01-1.28, trend test p value 0.01; fatal 1.14, 1.00-1.30, trend test p value 0.01). When associations were analyzed separately by geographical region (North America vs. other continents), positive associations between unprocessed red meat and egg intake, and inverse associations between poultry intake and advanced, advanced(r) and fatal cancers were limited to North American studies. However, differences were only statistically significant for eggs. Observed differences in associations by geographical region warrant further investigation.

Trichomonas vaginalis infection and risk of advanced prostate cancer.

The epidemiologic evidence for an association of Trichomonas vaginalis (Tv) with overall prostate cancer is mixed, but some studies suggest Tv may increase risk of more aggressive disease. The aim of this study was to assess whether Tv serostatus is associated with advanced or fatal prostate cancer. A total of 146 men with advanced (metastatic or fatal) prostate cancer and 181 age-matched controls were selected from two prior population-based, case-control studies. Tv serostatus was determined with the same laboratory methods used in previous epidemiologic studies. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using multivariable logistic regression to compare Tv serostatus in prostate cancer cases and controls adjusted for potential confounders. The seroprevalence of Tv in controls was 23%. Tv serostatus was not associated with an increased risk of metastatic or fatal prostate cancer (ORs < 1). Our study does not support an increased risk of advanced or fatal prostate cancer in men seropositive for Tv.

Male Pattern Baldness in Relation to Prostate Cancer-Specific Mortality: A Prospective Analysis in the NHANES I Epidemiologic Follow-up Study.

We used male pattern baldness as a proxy for long-term androgen exposure and investigated the association of dermatologist-assessed hair loss with prostate cancer-specific mortality in the first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. From the baseline survey (1971-1974), we included 4,316 men who were 25-74 years of age and had no prior cancer diagnosis. We estimated hazard ratios and used Cox proportional hazards regressions with age as the time metric and baseline hazard stratified by baseline age. A hybrid framework was used to account for stratification and clustering of the sample design, with adjustment for the variables used to calculate sample weights. During follow-up (median, 21 years), 3,284 deaths occurred; prostate cancer was the underlying cause of 107. In multivariable models, compared with no balding, any baldness was associated with a 56% higher risk of fatal prostate cancer (hazard ratio = 1.56; 95% confidence interval: 1.02, 2.37), and moderate balding specifically was associated with an 83% higher risk (hazard ratio = 1.83; 95% confidence interval: 1.15, 2.92). Conversely, patterned hair loss was not statistically significantly associated with all-cause mortality. Our analysis suggests that patterned hair loss is associated with a higher risk of fatal prostate cancer and supports the hypothesis of overlapping pathophysiological mechanisms.

Body mass index at mCRPC, weight change, and survival in advanced prostate cancer.

270 Background: Body mass index (BMI) at diagnosis is associated with increased risk of fatal prostate cancer, but the link between BMI at mCRPC and cancer progression is less clear. Cachexia, often defined as involuntary weight loss &gt; 5% over 6 months, is common in advanced cancers. The goal of this study was to examine the link between BMI at mCRPC and weight change as it relates to cancer progression, the outcomes of survival, and treatment use in a single-institution setting. Methods: 58 mCRPC patients treated at Tulane Hospital were identified, 41 of whom had an overweight BMI at mCRPC (BMI &gt; 25) and 17 with normal BMI at mCRPC (BMI &lt; 25). All patients had a confirmed prostate cancer death. Survival, treatment history, and percent weight change were compared according to BMI status. Rate of percent weight change was defined as the change in weight per day, from date of mCRPC diagnosis to the last treatment stop date or death date (“mCRPC days”). Linear regression, overall survival (OS), and nonparametric analyses were performed. Results: There was no significant difference between the normal and overweight BMI groups in overall survival, from date of diagnosis to death (median = 1835 days vs. 2710 days respectively). Additionally, the difference in survival from mCRPC to death was not statistically significant (median = 630 days vs. 799 days, p = 0.115). Use of Taxotere was not significantly different (47% vs. 68% respectively); however, overweight patients (n = 28) more likely received Abiraterone than normal BMI patients (n = 2) (p-value = 0.0001). The rate of percent weight change was significantly different for normal and overweight patients (mean = –0.050%/day vs. –0.019%/day, p = 0.003). Linear regression analysis showed that mCRPC days had a significant effect on percent weight change (p = 0.0109), and this effect was not significantly different between BMI groups (p = 0.6991). Conclusions: Survival after mCRPC was not significantly different between BMI groups. We observed a significant effect of mCRPC days on percent weight change, with a similar effect for both BMI groups. This outcome is expected, as more time would allow for greater weight changes to occur. Larger studies are needed to fully evaluate these observations.

Obesity and renal cancer incidence and mortality--a systematic review of prospective cohort studies.

There have been many studies published recently on obesity and the risk of renal cancer; however, the epidemiological evidence for such an association has not been consistent. Therefore, a systematic review was conducted of the prospective cohort studies to assess the association between obesity and the risk of renal cancer incidence and death. A search was conducted of the PubMed database and references to published studies from inception until May 2013. Guidelines for Assessing Quality in Prognostic Studies on the Basis of Framework for Potential Biases were followed for quality assessment of studies included in the systematic review. Twenty eligible studies were identified and included in the systematic review. Among the 20 selected studies, overall study quality was high. Although the evidence from the prospective cohort studies, linking obesity with renal cancer incidence, has not been entirely consistent, there is a convincing body of data for a positive relationship. Moreover, cumulative data is compelling for a strong positive association between obesity and fatal renal cancer. There is a relatively consistent amount of evidence that obesity increases the risk of renal cancer and fatal renal cancer. Further research is needed as better understanding of mechanisms by which obesity may influence renal cancer development and progression will aid the fostering of strategies for prevention and treatment of one of the most lethal human malignancies.

HRT for menopause: a delicate balance

First NICE guideline on menopause weighs up benefits and risks of HRT. Jennifer Thorley reports. Breast cancer and hormone-replacement therapy in the Million Women StudyCurrent use of HRT is associated with an increased risk of incident and fatal breast cancer; the effect is substantially greater for oestrogen-progestagen combinations than for other types of HRT. Full-Text PDF