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Men with clinical stage T3a disease are at high risk and are often encouraged to undergo radiation therapy with concomitant hormonal therapy. The long‐term outcomes among men treated with radical prostatectomy for clinical stage T3a disease were examined.Among 3397 men treated by radical prostatectomy by 1 surgeon between 1987 and 2003, 62 (1.8%) men were identified who had clinical stage T3a disease. Among the 56 men not treated with neoadjuvant or adjuvant therapies before prostate‐specific antigen (PSA) recurrence, the long‐term outcomes of PSA‐free survival, metastasis‐free survival, and prostate cancer specific survival were examined. Median and mean follow‐up after surgery were 10.3 and 13 years, respectively (range, 1–17).Ninety‐one percent of men in this group had pathological T3 disease. PSA‐free survival at 15 years after surgery was 49%. Metastasis‐free survival and cause‐specific survival at 15 years after surgery were 73% and 84%, respectively. Among men with a PSA recurrence, 46% received secondary therapy before metastasis. The only preoperative or pathological feature that predicted risk of prostate cancer death was lymph node metastasis (hazard ratio [HR]: 9.22, 95% confidence interval [CI]: 1.06–80.02, P = .044). Among the 28 men with a PSA recurrence, PSA doubling time (PSADT) data were available for 23, of which 11 (48%) has a PSADT ≥9 months. No patient with a PSADT ≥9 months died of prostate cancer. A PSADT <9 months was significantly associated with increased risk of prostate cancer death (log‐rank, P = .004).In a select cohort of men with clinical stage T3a disease, radical prostatectomy alone provides long‐term cancer control in about half of the men and results in a prostate cancer‐specific survival of 84%. Among men with a PSA recurrence, PSADT at the time of recurrence is a useful determinant of risk of prostate cancer death. Cancer 2007. © 2007 American Cancer Society. [ABSTRACT FROM AUTHOR]

CYP1A1 is likely to play an important role in the etiology of CaP through its function in activating environmental procarcinogens and catalyzing the oxidative metabolites of estrogens. To test the hypothesis that genetic polymorphisms in the CYP1A1 gene may be associated with the risk for CaP, we compared the allele, genotype and haplotype frequencies of 3 SNPs (3801T>C, 2455A>G and 2453C>A) of CYP1A1 among 159 HPC probands, 245 sporadic CaP cases and 222 unaffected men. Two SNPs (3801T>C and 2455A>G) were each individually associated with CaP risk when the allele and genotype frequencies were compared between CaP patients and unaffected controls. Furthermore, a combined SNP analysis using a haplotype approach revealed an even stronger association in Caucasians. Specifically, 4 major haplotypes (T-A-C, C-A-C, C-G-C and T-A-A) accounted for 99.8% of all observed haplotypes. These 4 haplotypes correspond to the previously described nomenclature (CYP1A1*1A, CYP1A1*2A, CYP1A1*2B and CYP1A1*4). The frequencies of these 4 haplotypes were significantly different among CaP patients and controls. The haplotype T-A-C (CYP1A1*1A) was significantly associated with increased risk for CaP, and the haplotype C-A-C (CYP1A1*2A) was significantly associated with decreased risk for CaP. These findings suggest that genetic polymorphisms in CYP1A1 may modify the risk for CaP. © 2003 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]