Format

Send to

Choose Destination
See comment in PubMed Commons below
Ann Surg Oncol. 2010 Jun;17(6):1675-81. doi: 10.1245/s10434-010-0994-3. Epub 2010 Mar 4.

Clinical significance of tumor necrosis factor receptor superfamily member 11b polymorphism in prostate cancer.

Author information

1
Department of Pharmacy, China Medical University, Taichung, Taiwan.

Abstract

BACKGROUND:

Bone metastases are the most critical complication of prostate cancer (PCa), resulting in severe morbidity and mortality. Tumor necrosis factor receptor superfamily member 11b (TNFRSF11B) is a critical regulator between PCa cells and the bone environment. Recently, TNFRSF11B rs10505346 has been implicated in PCa risk in the Cancer Genetic Markers of Susceptibility genomewide association study. However, the association between this variant and biochemical failure in PCa patients receiving radical prostatectomy (RP) has not been determined.

METHODS:

Associations of TNFRSF11B rs10505346 with age at diagnosis, preoperative prostate-specific antigen (PSA) level, Gleason score, pathologic stage, surgical margin, and PSA recurrence were evaluated in a cohort of 314 localized PCa patients receiving RP. The prognostic significance on PSA recurrence was assessed by Kaplan-Meier analysis and Cox regression model.

RESULTS:

The mean level of preoperative PSA and the relative risks of PSA recurrence after RP were lower in individuals with T allele than in those with the G allele at TNFRSF11B rs10505346 (P = 0.019 and 0.014, respectively). The T allele of rs10505346 remained a protective factor against PSA recurrence (P = 0.022) in multivariate Cox regression model after considering all clinicopathological risk factors except PSA level.

CONCLUSIONS:

Our data suggest that TNFRSF11B rs10505346 is associated with PSA level and might be a prognostic factor for the recurrence of PSA in PCa patients receiving RP.

PMID:
20204532
DOI:
10.1245/s10434-010-0994-3
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center