Aims: The tumor suppressor p53 plays a major role in stress responses of the cell and modulates cell cycle arrest and apoptosis. The p53 R72P SNP (G/C) was found to be associated with increased risk of various malignancies. However, for prostate cancer only limited data are available, especially in Caucasian population. We therefore analysed the distribution of the R72P SNP in male Caucasian prostate cancer patients and a healthy control group.

Methods: Peripheral blood or normal prostate tissue from formalin-fixed, paraffin-embedded tissue sections were used for DNA isolation. Allelic variants of p53 Codon 72 SNP were determined using RFLP analysis. Overall, 194 male patients without any malignancy (mean age 67,3 ±10,6, range 34-88) and 118 male consecutive prostate cancer patients (mean age 64,2 ±6,0, range 46-74) were investigated.

Results: The distribution of the p53 R72P SNP did not differ significantly between prostate cancer patients and the control group (Cases GG 55.1%, GC 37.3%, CC 7.6%; Controls GG 53.6%, GC 40.7%, CC 5.7%). There was also no association between the allelic variants and Gleason score (Gleason sum < 7 GG 61.2%, GC 32.7%, CC 6.1%; Gleason sum ≥ 7 GG 53.3%, GC 38.3%, CC 8.3%). Significant difference in the distribution of the R72P SNP regarding onset of the disease was found (p=0,035), showing increased frequency of the proline variant in younger patients (Age ≤ 60 GG 37%, GC 3.7%, CC 59.3%; Age > 60 GG 60.7%, GC 8.3%, CC 31%). Regarding recurrence, a trend towards increase of the G-allele was found in patients with early recurrence (Cases with recurrence GG 81.3%, GC + CC 18.7%, Cases with recurrence GG 50%, GC + CC 50%, p=0.039).

Conclusions: The overall risk of prostate cancer is not associated with R72P SNP. However, disease onset might be modulated by the p53 variant allele suggesting an important role of apoptosis regulation in prostate carcinogenesis.

Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1840.

©2010 American Association for Cancer Research
2010