Telomere DNA Content in Prostate Biopsies Predicts Early Rise in Prostate-specific Antigen After Radical Prostatectomy for Prostate Cancer - 20/08/11
Reprint requests: Jeffrey K. Griffith, PhD, Department of Biochemistry and Molecular Biology, MSC 08 4670, 1 University of New Mexico, Albuquerque, NM 87131-0001Résumé |
Objective |
To determine whether measurement of telomere DNA content (TC) in prostate biopsy tissue predicts prostrate-specific antigen (PSA) recurrence in men after undergoing radical prostatectomy for prostate cancer.
Methods |
Slot blot titration assay was used to quantitate TC in archived diagnostic prostate needle biopsy specimens for subjects (n = 103) diagnosed with prostate cancer and who subsequently underwent radical prostatectomy between 1993 and 1997. TC was compared to the clinical outcome measure; PSA recurrence, defined as an increase in PSA ≥ 0.2 ng/mL on 2 or more consecutive measurements post-prostatectomy, was observed retrospectively, for a mean follow-up period of 114 months (range, 1-165).
Results |
In the cohort, 46 subjects had a PSA recurrence. In a univariate Cox proportional hazards model, low TC (<0.3 of standard) demonstrated a significant risk for PSA recurrence (HR = 1.94; 95% CI: 1.02-3.69, P = .04). In a subset analysis of men with biopsy Gleason sum ≤ 6 (n = 63; 25 recurrences), a univariate Cox proportional hazards model demonstrated that low TC had a greater risk of PSA recurrence (HR = 4.53; 95% CI: 2.00-10.2, P < .01). In a multivariate Cox proportional hazards model, low TC was also significantly associated with PSA recurrence in this subset after controlling for preoperative PSA levels (HR = 6.62; 95% CI: 2.69-16.3, P < .01).
Conclusions |
Low TC measured in prostate biopsy tissue predicts early likelihood of post-prostatectomy PSA recurrence in a retrospective analysis, and in men with biopsy Gleason sum ≤ 6 disease it is also independent of preoperative PSA level.
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| Eric G. Treat and Christopher M. Heaphy contributed equally to this study. |
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| Supported by National Institutes of Health Grant RR0164880 (to M. B. and J. K. G.), Department of Defense pre-doctoral training awardW81XWH-05-0273 (to C. M. H.), University of New Mexico Cancer Center Support Grant NIH/NCI P30CA118110, and the University of New Mexico General Clinical Research Center (NIH NCRR GCRC Grant M01-RR00997) (to E. G. T.). |
Vol 75 - N° 3
P. 724-729 - mars 2010 Retour au numéro
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