Combined analysis of EGF+61G > A and TGFB1+869T > C functional polymorphisms in the time to androgen independence and prostate cancer susceptibility

• Type: Article in International Scientific Journal
• Date: 2009

Authors

Teixeira, AL (Author) Other; Ribeiro, R (Author) Other; Morais, A (Author) Other; Lobo, F (Author) Other; Fraga, A (Author) Other; Pina, F (Author) Other; Calais da Silva, FM (Author) Other; Calais da Silva, FE (Author) Other; Medeiros, R (Author) ICBAS

Journal

Title: Pharmacogenomics Journal

Vol. 9

Pages: 341-346

ISSN: 1470-269X

Publisher: Springer Nature

Indexing

ISI Web of Knowledge - 16 Citations

Scopus - 16 Citations

Scientific classification

FOS: Medical and Health sciences > Basic medicine

Other information

Authenticus ID: P-003-FJW

DOI: 10.1038/tpj.2009.20

Abstract (EN): Proliferative mechanisms involving the epidermal growth factor (EGF) and transforming growth factor beta (TGF-beta(1)) ligands are potential alternative pathways for prostate cancer (PC) progression to androgen independence (AI). Thus, the combined effect of EGF and TGFB1 functional polymorphisms might modulate tumor microenvironment and consequently its development. We studied EGF + 61G>A and TGFB1 + 869T>C functional polymorphisms in 234 patients with PC and 243 healthy individuals. Intermediate-and high-proliferation genetic profile carriers have increased risk for PC (odds ratio (OR) = 3.76, P = 0.007 and OR = 3.98, P = 0.004, respectively), when compared with low proliferation individuals. Multivariate analysis showed a significantly lower time to AI in the high proliferation group, compared with the low/intermediate proliferation genetic profile carriers (HR = 2.67, P = 0.039), after adjustment for age, metastasis and stage. Results suggest that combined analysis of target genetic polymorphisms may contribute to the definition of cancer susceptibility and pharmacogenomic profiles. Combined blockage of key molecules in proliferation signaling pathways could be one of the most promising strategies for androgen-independent prostate cancer. The Pharmacogenomics Journal (2009) 9, 341-346; doi:10.1038/tpj.2009.20; published online 2 June 2009

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 6