title: Influence of body mass index on prostate-specific antigen failure after androgen suppression and radiation therapy for localized prostate cancer.
abstract: BACKGROUND
  Increasing body mass index (BMI) is associated with shorter time to prostate-specific antigen (PSA) failure after radical prostatectomy. Whether BMI is associated with time to PSA failure was investigated in men treated with androgen suppression therapy (AST) and radiation therapy (RT) for clinically localized prostate cancer.
  
  
  METHODS
  The observational prospective cohort study consisted of 102 men with clinically localized prostate cancer who received 70 Gy RT with 6 months of AST on a single arm of a randomized trial between December 1995 and April 2001. Height and weight data were available at baseline for 99 (97%) of the men, from which BMI was calculated. Adjusting for age (continuous) and known prognostic factors including PSA level (continuous), Gleason score, and T-category, Cox regression analyses were performed to analyze whether BMI (continuous) was associated with time to PSA failure (PSA >1.0 ng/mL and increasing >0.2 ng/mL on 2 consecutive visits).
  
  
  RESULTS
  Median age and median BMI (interquartile range [IQR]) at baseline was 72 (69.1-74.7) years and 27.4 (24.8-30.7) kg/m,(2) respectively. In addition to an increasing PSA level (P = .006) and Gleason 8-10 cancer (P = .024), after a median follow-up (IQR) of 6.9 (5.6-8.5) years, an increasing BMI was also significantly associated with a shorter time to PSA failure (adjusted hazard ratio [HR]: 1.10; 95% confidence interval [CI]: 1.01-1.19; P = .026) after RT and AST.
  
  
  CONCLUSIONS
  After adjusting for known prognostic factors, baseline BMI is significantly associated with time to PSA failure after RT and AST for men with clinically localized prostate cancer. Further study is warranted to assess the impact of an increasing BMI after AST administration on PSA failure, prostate cancer-specific, and all-cause mortality.
authors.affiliation: Department of Radiation Oncology, Brigham and Women's Hospital and Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA. jefstathiou@partners.org
authors.forename: Jason A
authors.initials: JA
authors.lastname: Efstathiou
authors.forename: Ming-Hui
authors.initials: MH
authors.lastname: Chen
authors.forename: Andrew A
authors.initials: AA
authors.lastname: Renshaw
authors.forename: Marian J
authors.initials: MJ
authors.lastname: Loffredo
authors.forename: Anthony V
authors.initials: AV
authors.lastname: D'Amico
mesh_terms: D000230:Adenocarcinoma / Q000628:therapy*; D000368:Aged; D000726:Androgen Antagonists / Q000627:therapeutic use*; D018931:Antineoplastic Agents, Hormonal; D015992:Body Mass Index; D015331:Cohort Studies; D003131:Combined Modality Therapy; D006801:Humans; D008297:Male; D017430:Prostate-Specific Antigen / Q000097:blood*; D011471:Prostatic Neoplasms / Q000628:therapy*; D020266:Radiotherapy, Conformal; D012307:Risk Factors; D016896:Treatment Outcome
chemical_list: D000726:Androgen Antagonists; D018931:Antineoplastic Agents, Hormonal; D017430:Prostate-Specific Antigen