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Valicenti RK, DeSilvio M, Hanks GE, Porter A, Brereton H, Rosenthal SA, Shipley WU, Sandler HM, Haile RW, Thomas DC, McGuire V, Felberg A, John EM, Milne RL, Hopper JL, Jenkins MA, Levine AJ, Daly MM, Buys SS, Senie RT, Andrulis IL, Knight JA, Godwin AK, Southey M, McCredie MR, Giles GG, Andrews L, Tucker K, Miron A, Apicella C, Tesoriero A, Bane A, Pike MC, Whittemore AS
Posttreatment prostatic-specific antigen doubling time as a surrogate endpoint for prostate cancer-specific survival: An analysis of radiation therapy oncology group protocol 92-02 BRCA1 and BRCA2 mutation carriers, oral contraceptive use, and breast cancer before age 50
INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE prostate cancer; prostate-specific antigen doubling time; mortality; surrogate endpoint (2006) 15:1863-1870.
Background: Understanding the effect of oral contraceptives on risk of breast cancer in BRCA1 or BRCA2 mutation carriers is important because oral contraceptive use is a common, modifiable practice. Methods: We studied 497 BRCA1 and 307 BRCA2 mutation carriers, of whom 195 and 128, respectively, had been diagnosed with breast cancer. Case-control analyses were conducted using unconditional logistic regression with adjustments for family history and familial relationships and were restricted to subjects with a reference age under 50 years. Results: For BRCA1 mutation carriers, there was no significant association between risk of breast cancer and use of oral contraceptives for at least 1 year [odds ratio (OR), 0.77; 95% confidence interval (95% CI), 0.53-1.12] or duration of oral contraceptive use (P-trend = 0.62). For BRCA2 mutation carriers, there was no association with use of oral contraceptives for at least 1 year (OR, 1.62; 95% CI, 0.90-2.92); however, there was an association of elevated risk with oral contraceptive use for at least 5 years (OR, 2.06; 95% CI, 1.08-3.94) and with duration of use (ORtrend per year of use, 1.08; P = 0.008). Similar results were obtained when we considered only use of oral contraceptives that first started in 1975 or later. Conclusions: We found no evidence overall that use of oral contraceptives for at least 1 year is associated with breast cancer risk for BRCA1 and BRCA2 mutation carriers before age 50. For BRCA2 mutation carriers, use of oral contraceptives may be associated with an increased risk of breast cancer among women who use them for at least 5 years. Further studies reporting results separately for BRCA1 and BRCA2 mutation carriers are needed to resolve this important issue. C1 Univ So Calif, Dept Prevent Med, Calif Keck Sch Med, Los Angeles, CA 90089 USA. Stanford Univ, Sch Med, Dept Hlth Res & Policy, Stanford, CA 94305 USA. No Calif Canc Ctr, Fremont, CA USA. Early Detect Lab, Melbourne, Vic, Australia. Univ Melbourne, Melbourne, Vic, Australia. Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Univ Utah, Dept Hematol Oncol, Salt Lake City, UT USA. Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA. Mt Sinai Hosp, Canc Care Ontario, Toronto, ON M5G 1X5, Canada. Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada. Univ Otago, Dunedin, New Zealand. Canc Council Victoria, Canc Epidemiol Ctr, Carlton, Vic, Australia. Prince Wales Univ, Hereditary Canc Clin, Sydney, NSW, Australia. Harvard Univ, Sch Med, Dept Canc Biol, Dana Farber Canc Inst, Boston, MA 02115 USA. Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
MeSH terms
randomized treatment was a significant predictor for CSS (p(Cox) = MORTALITY RADICAL PROSTATECTOMY DEATH WOMEN GENE OVARIAN-CANCER RISK EPIDEMIOLOGY RISK AB (Purpose:) under bar We evaluated whether posttreatment prostatic-specific antigen doubling time (PSADT) was predictive of prostate cancer mortality by testing the Prentice requirements for a time to PSADT (assuming first-order kinetics for a minimum of 3 rising PSADT < 6 months (pc < 0001) 0002)-PSADT < 9 months (P-Cox < and PSADT < 12 months (P-Cox < 0001) but not for PSADT < 3 0001) (P-Cox = 04) The significant posttreatment PSADTs were also significant predictors of CSS (P-Cox < 0001) After adjusting for T Gleason score and PSA stage-all of Prentice's requirements were not indicating that the effect of PSADT on CSS was not independent of met the randomized treatment (Conclusions) under bar Prostatic specific antigen doubling time is but did not meet all of Prentice's significantly associated with CSS the risk of dying requirements for a surrogate endpoint of CSS Thus of prostate cancer is not fully explained by PSADT (c) 2006 Elsevier Inc NONCARRIERS REGISTRY HISTORY surrogate endpoint FAILURE (Results: ) under bar After a median follow-up time of 59 years PCR RECURRENCE PSA measurements) and cancer-specific survival (CSS) (Methods and Materials: ) under bar We analyzed posttreatment PSA 514 men with localized prostate cancer measurements in a cohort of 1 (T2c-4 and PSA level < 150 ng treated and monitored prospectively mL) on Radiation Therapy Oncology Group Protocol 92-02 From June 1992 to men were randomized to neoadjuvant androgen deprivation and April 1995 or in combination with 24 65-70 Gy of radiation therapy (n = 761) months of adjuvant androgen deprivation (n = 753) Using an adjusted we tested if PSADT was prognostic and Cox proportional hazards model independent of randomized treatment in this cohort The endpoints were
Publication Date: 2006-10-01.
Last updated on Thursday, July 09, 2020