PRSS55 – Prostate Cancer

PRSS55 has emerged as a genetic risk factor in prostate cancer, with evidence accrued from multi-patient association studies that evaluated polymorphisms in angiogenic pathway genes. In two independent case‑control studies, allelic variants in genes including PRSS55 were examined alongside other angiogenesis‑related markers, where risk alleles were associated with an increased likelihood of prostate cancer (PMID:17175378) and a significant gene‑dosage effect was reported (PMID:17917789).

The genetic evidence is supported by statistically significant associations in cohorts comprising over 100 prostate cancer patients, underscoring the contribution of PRSS55 risk alleles to disease susceptibility. Although segregation data of affected family members is not available in these case‑control analyses, the consistent detection of risk alleles across diverse populations enhances the strength of evidence.

Mechanistic insights further bolster the association, with functional studies indicating that modulation of angiogenic signaling may play a critical role in prostate tumor biology. In one study investigating beta‑1 integrin cytoplasmic variants, altered expression of thrombospondin‑1 was shown to impact cellular proliferation in prostate cancer models, thereby providing a plausible mechanistic link by which PRSS55‑related pathways could influence cancer aggressiveness (PMID:19549894).

Integration of the genetic and experimental data yields a strong narrative for the involvement of PRSS55 in prostate cancer development. Although the genetic evidence predominantly comes from association studies and does not represent a classical Mendelian inheritance pattern, the consistent replication of risk effects across independent cohorts is compelling. The functional experiments, while supportive, are indirect but consistent with the overall concept of angiogenic dysregulation in prostate cancer.

The overall clinical validity between PRSS55 and prostate cancer is rated as Strong, based on statistically robust case‑control studies and mechanistic support from functional assays. This integration of evidence aids diagnostic decision‑making and underpins the translational potential for further research and eventual commercial application.

Key Take‑home: The convergent genetic and functional evidence makes PRSS55 a promising candidate for risk stratification in prostate cancer.

References

• Cancer genetics and cytogenetics • 2007 • TSP1 and MMP9 genetic variants in sporadic prostate cancer PMID:17175378
• Molecular biology reports • 2009 • Combined effects of the angiogenic genes polymorphisms on prostate cancer susceptibility and aggressiveness PMID:17917789
• Cancer research • 2009 • Beta1 integrin cytoplasmic variants differentially regulate expression of the antiangiogenic extracellular matrix protein thrombospondin 1 PMID:19549894

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