Time filter

Source Type

Eisenberg M.L.,Stanford University | Betts P.,Cancer Epidemiology and Surveillance Branch | Herder D.,Baylor College of Medicine | Lamb D.J.,Baylor College of Medicine | Lipshultz L.I.,Baylor College of Medicine
Fertility and Sterility | Year: 2013

Objective: To determine whether men with azoospermia are at an elevated risk of developing cancer in the years following an infertility evaluation. Design: Cohort study. Setting: United States andrology clinic. Patient(s): A total of 2,238 men with complete records were evaluated for infertility at a single andrology clinic in Texas from 1989 to 2009. Intervention(s): None. Main Outcome Measure(s): Cancer incidence was determined by linkage to the Texas Cancer Registry. Result(s): In all, 451 men had azoospermia, and 1,787 were not azoospermic, with a mean age at infertility evaluation of 35.7 years. Compared with the general population, infertile men had a higher risk of cancer, with 29 cases observed compared with 16.7 expected (standardized incidence rate [SIR] 1.7, 95% confidence interval [CI] 1.2-2.5). When stratifying by azoospermia status, azoospermic men had an elevated risk of cancer (SIR 2.9, 95% CI 1.4-5.4). Infertile men without azoospermia had a trend toward a higher rate of cancer (SIR 1.4, 95% CI 0.9-2.2). The Cox regression model revealed that azoospermic men had 2.2-fold higher cancer risk compared with nonazoospermic men (hazard ratio 2.2, 95% CI 1.0-4.8). Conclusion(s): Men with azoospermia have an increased risk of subsequently developing cancer, suggesting a possible common etiology between azoospermia and cancer development. Additional follow-up of azoospermic men after reproductive efforts end may be warranted. © 2013 by American Society for Reproductive Medicine. Source

White A.,University of Texas Health Science Center at Houston | Coker A.L.,University of Kentucky | Du X.L.,University of Texas Health Science Center at Houston | Eggleston K.S.,University of Texas Health Science Center at Houston | Williams M.,Cancer Epidemiology and Surveillance Branch
Cancer | Year: 2011

BACKGROUND: To the authors' knowledge, few studies to date have examined racial differences in prostate cancer survival while controlling for socioeconomic status (SES). No such studies have examined this association in Texas, a large state with significant ethnic and racial diversity. The objective of this analysis was to determine whether racial disparities in survival for men diagnosed with prostate cancer in Texas from 1995 through 2002 remained after adjusting for SES, rural residence, and stage of disease. METHODS: A cohort of 87,449 men who were diagnosed with prostate cancer was identified from the Texas Cancer Registry. The SES measure was based on census tract data reflecting median household income, median home value, and percentages of men living below poverty, with a college education, and with a management or professional occupation. The 5-year survival rates were calculated using the Kaplan-Meier method and Cox proportional hazard modeling was used to estimate hazard ratios (HRs) for race and all-cause and disease-specific mortality. RESULTS: After adjusting for SES, age, stage of disease, tumor grade, year of diagnosis, and rural residence, both black and Hispanic men were more likely (adjusted HR [aHR], 1.70 [95% confidence interval (95% CI), 1.58-1.83] and aHR, 1.11 [95% CI, 1.02-1.20], respectively) to die of prostate cancer compared with white men. The pattern of survival disadvantage for black men held for those diagnosed with localized disease and advanced disease, and for those with an unknown stage of disease at diagnosis. CONCLUSIONS: Substantial racial disparities in prostate cancer survival were found for men in Texas. Future studies should incorporate treatment data as well as comorbid conditions because this information may explain noted survival disparities. © 2010 American Cancer Society. Source

Ognjanovic S.,University of Minnesota | Carozza S.E.,Oregon State University | Chow E.J.,Fred Hutchinson Cancer Research Center | Fox E.E.,Cancer Epidemiology and Surveillance Branch | And 7 more authors.
British Journal of Cancer | Year: 2010

Background: Little is known about risk factors for childhood rhabdomyosarcoma (RMS) and the histology-specific details are rare.Methods: Case-control studies formed by linking cancer and birth registries of California, Minnesota, New York, Texas and Washington, which included 583 RMS cases (363 embryonal and 85 alveolar RMS) and 57 966 randomly selected control subjects, were analysed using logistic regression. The associations of RMS (overall, and based on embryonal or alveolar histology) with birth weight across five 500 g categories (from 2000 to 4500 g) were examined using normal birth weight (2500-3999 g) as a reference. Large (>90th percentile) and small (<10th percentile) size for gestational age were calculated based on birth weight distributions in controls and were similarly examined.Results: High birth weight increased the risk of embryonal RMS and RMS overall. Each 500 g increase in birth weight increased the risk of embryonal RMS (odds ratio (OR)1.27, 95% confidence interval (CI)1.14-1.42) and RMS overall (OR1.18, 95% CI1.09-1.29). Large size for gestational age also significantly increased the risk of embryonal RMS (OR1.42, 95% CI1.03-1.96).Conclusions: These data suggest a positive association between accelerated in utero growth and embryonal RMS, but not alveolar RMS. These results warrant cautious interpretation owing to the small number of alveolar RMS cases. © 2010 Cancer Research UK All rights reserved. Source

Litvinov I.V.,McGill University | Tetzlaff M.T.,University of Houston | Rahme E.,McGill University | Habel Y.,McGill University | And 7 more authors.
Cancer | Year: 2015

BACKGROUND Cutaneous T-cell lymphomas (CTCLs) (mycosis fungoides and its leukemic variant, Sezary syndrome) are rare malignancies. Reports of the occurrence of mycosis fungoides in married couples and families raise the possibility of an environmental trigger for this cancer. Although it has been suggested that CTCL arises from inappropriate T-cell stimulation, to the authors' knowledge no preventable trigger has been identified to date. METHODS Using region, zip code, age, sex, and ethnicity, the authors analyzed the demographic data of 1047 patients from Texas who were seen in a CTCL clinic at The University of Texas MD Anderson Cancer Center during 2000 through 2012 (the MDACC database) and 1990 patients who were recorded in the population-based Texas Cancer Registry between 1996 and 2010. Subsequently, data from both databases were cross-analyzed and compared. RESULTS The current study findings, based on the MDACC database, documented geographic clustering of patients in 3 communities within the Houston metropolitan area, in which CTCL incidence rates were 5 to 20 times higher than the expected population rate. Analysis of the Texas Cancer Registry database defined the CTCL population rate for the state to be 5.8 cases per million individuals per year (95% confidence interval, 5.5-6.0 per million individuals per year), thus confirming the observations from the MDACC database and further highlighting additional areas of geographic clustering and regions spared from CTCL in Texas. CONCLUSIONS The current study documented geographic clustering of CTCL cases in Texas and argued for the existence of yet unknown external causes/triggers for this rare malignancy. Cancer 2015;121:1993-2003. © 2015 American Cancer Society. Source

Eisenberg M.L.,Stanford University | Li S.,Stanford University | Betts P.,Cancer Epidemiology and Surveillance Branch | Herder D.,Baylor College of Medicine | And 2 more authors.
BJU International | Year: 2015

Objective: To determine if testosterone therapy (TT) status modifies a man's risk of cancer. Patients and Methods: The Urology clinic hormone database was queried for all men with a serum testosterone level and charts examined to determine TT status. Patient records were linked to the Texas Cancer Registry to determine the incidence of cancer. Men accrued time at risk from the date of initiating TT or the first office visit for men not on TT. Standardised incidence rates and time to event analysis were performed. Results: In all, 247 men were on TT and 211 did not use testosterone. In all, 47 men developed cancer, 27 (12.8%) were not on TT and 20 (8.1%) on TT. There was no significant difference in the risk of cancer incidence based on TT (hazard ratio [HR] 1.0, 95% confidence interval [CI] 0.57-1.9; P = 1.8). There was no difference in prostate cancer risk based on TT status (HR 1.2, 95% CI 0.54-2.50). Conclusion: There was no change in cancer risk overall, or prostate cancer risk specifically, for men aged >40 years using long-term TT. © 2014 The Authors. BJU International © 2014 BJU International. Source

Discover hidden collaborations