Abstract
status was determined by FISH. TMPRSS2:ERG status was also determined by FISH. Differences in demographics, clinical and pathologic factors were compared with Chi-squared tests between controls and cases with and without PTEN loss. The hazard ratio for PCa recurrence/progression was determined with age-adjusted and multivariate Cox proportional hazard analyses adjusting for age, family history of PCa, TMPRSS2:ERG status, smoking status, BMI, PSA, Gleason sum and stage. RESULTS: Of the 496 cases with evaluable PTEN status, PTEN loss was present in 68 (14%). A family history of prostate cancer was seen in 11%, 16% and 24% of controls, cases with PTEN loss and cases with PTEN normal tumors, respectively (p < 0.01 ). As PSA at diagnosis increased, patients were more likely to have PTEN loss (p < 0.01). In prostate cancer cases, PTEN loss was more common in those with the TMPRSS2:ERG gene fusion (22%) than those without TMPRSS2:ERG re-arrangement (7%, p < 0.01). Recurrence/progression data were available for 379 cases and such events were observed in 21% and 35% of PTEN normal and PTEN loss patients (p 1⁄4 0.036). In the age-adjusted model, PTEN loss was associated with a 72% increased risk of disease recurrence/progression compared to cases with normal PTEN (HR 1.72, 95% CI 1.02 e 2.89), although this estimate was attenuated in the multivariate model, (adjusted HR 1.63, 95% CI 0.91-2.95). CONCLUSIONS: PTEN loss was observed in 14% of cases with localized prostate cancer undergoing RP, yet PTEN loss was associated with a higher risk of recurrence/progression. Men with a family history of prostate cancer less commonly had PTEN loss whereas loss of PTEN was more commonly observed in patients with the TMPRSS2:ERG gene fusion. Further studies into the role of PTEN loss in the earlier stages of prostate carcinogenesis may be warranted.
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