The I/D polymorphism of angiotensin I – converting enzyme gene in patients with prostate cancer
Article published in Urologia Polska 2008/61/Supl. 1.

authors

Artur Lemiński, Agnieszka Bińczak-Kuleta, Mariusz Kaczmarczyk, Magdalena Ostanek, Karolina Skonieczna, Maja Krzyształowska, Beata Łoniewska, Andrzej Ciechanowicz, Andrzej Sikorski

Katedra i Klinika Urologii, PAM w Szczecinie
Katedra Diagnostyki Laboratoryjnej i Medycyny Molekularnej, PAM w Szczecinie
Klinika Patologii Noworodka, PAM w Szczecinie

summary

Introduction.

The role of tissue renin-angiotensin system in pathogenesis and progression of prostate cancer is not fully understood. First type of angiotensin II receptor and angiotensin I-converting enzyme (ACE) are present in prostate cells. ACE produces angiotensin II - a potent vasoconstrictor, which stimulates proliferation and angiogenesis by means of influence on numerous growth factors. The ACE gene sequence contains a I/D polymorphism based on insertion (I) or deletion (D) of 287 BP within intron 16. DD homozygotes show doubled ACE activity in comparison with II homozygotes. Intermediate ACE levels are found in ID heterozygotes. There have been only two papers identifying an association between I/D ACE polymorphism and prostate cancer published to date.

Objectives.

To investigate an association between I/D ACE gene polymorphism and prostate cancer susceptibility, and to correlate some clinical features of this tumor with the ACE genetic variants.

Materials and methods.

The study was approved by local ethics committee. Written informed consent was obtained from 122 consecutive patients with pathologically confirmed prostate cancer, hospitalized in department of urology in Szczecin between 2004-2006. Population control group comprised genomic DNA isolated from umbilical cord blood samples of 96 male newborns born in the neonatology unit between 2004-2005. Genomic DNA was isolated from collected blood samples, and underwent amplification with PCR method using primers flanking the polymorphic region. ACE genotypes (II, ID or DD) were identified in picture of PCR products separated by electrophoresis on 3% agarose gel stained with ethidium bromide.

Results. ACE genotype distribution did not differ significantly between the study group: 25,41% (n=31) II, 51,64% (n=63) ID, 22,59% (n=28) DD, and controls: 27,08% (n=26) II, 47,92% (n=46) ID and 25,00% (n=24) DD. Genotype-phenotype analysis carried out in study group did not reveal any significant correlation between ACE genotype and following clinical features of prostate cancer: age at diagnosis, PSA level, prostate volume and Gleason score.

Conclusions.

Despite data from published papers, no significant differences in ACE genotype distribution between prostate cancer patients and population controls suggest lack of association of this polymorphism with prostate cancer susceptibility. Furthermore, assessed clinical features of prostate cancer show no remarkable correlation with I/D ACE polymorphism.