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[Cancer Research 61, 7375-7378, October 15, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

A Polymorphism in Endostatin, an Angiogenesis Inhibitor, Predisposes for the Development of Prostatic Adenocarcinoma1

Paula Iughetti, Oscar Suzuki, Paulo H. C. Godoi, Venâncio Avancini Ferreira Alves, Andrea L. Sertié, Todd Zorick, Fernando Soares, Anamaria Camargo, Eloísa S. Moreira, Celso di Loreto, Carlos Alberto Moreira-Filho, Andrew Simpson, Glaucius Oliva and Maria Rita Passos-Bueno2

Centro de Estudos do Genoma Humano, Departamento de Biologia, Instituto de Biociências, USP, São Paulo 05508-900 [P. I., O. S., A. L. S., T. Z., M. R. P-B.]; Instituto de Química de São Carlos, São Carlos 13560-970 [P. H. C. G.]; Departamento de Patologia, Faculdade de Medicina, USP 01246-903 [V. A. F. A., C. d. L.]; Instituto Ludwig, São Paulo 01509-010 [F. S., A. C., E. S. M.]; Departamento de Imunologia, Instituto de Ciências Biomédicas, USP [C. A. M-F.]; and Instituto de Física de São Carlos, USP, São Carlos 13560-970 [G. O.], Brazil

We have performed association studies between a novel coding single nucleotide polymorphism (D104N) in endostatin, one of the most potent inhibitors of angiogenesis, and prostate cancer. We observed that heterozygous N104 individuals have a 2.5 times increased chance of developing prostate cancer as compared with homozygous D104 subjects (odds ratio, 2.4; 95% confidence interval, 1.4–4.16). Modeling of the endostatin mutant showed that the N104 protein is stable. These results together with the observation that residue 104 is evolutionary conserved lead us to propose that: (a) the DNA segment containing this residue might contain a novel interaction site to a yet unknown receptor; and (b) the presence of N104 impairs the function of endostatin.




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