ABSTRACT 1528(P5-15)
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腎細胞癌と移行上皮癌でのbax遺伝子におけるframeshift mutationの欠損:ビリーム・ウラジーミル、川崎隆、高橋公太、冨田善彦 (新潟大学・医・泌)

Absence of frameshift mutations in the bax gene in renal cell cancer (RCC) and transitional cell cancer (TCC): Vladimir BILIM, Takashi KAWASAKI, Kota TAKAHASHI, and Yoshihiko TOMITA (Dept. of Urology, Niigata Univ., School of Med.)

Bax protein, a member of Bcl-2 family, regulates apoptotic pathway that involves both Bcl-2 and p53. It was shown, that alterations of p53 and bcl-2 are involved in tumorigenesis of transitional cell carcinoma (TCC), and renal cell carcinoma (RCC) correspondingly. Bcl-2 and Bax are downstream of p53 dependent apoptotic pathway. The ratio between Bax/Bcl-2 heterodimers and Bax/Bax homodimers appears to be pivotal in deciding the life or death of a cell. bax gene mutations are found in hematological malignancies, colon cancer with microsatellite mutator phenotype, and some other cancers. We therefore evaluated the possibility that Bax functions as TCC or RCC tumor suppressor gene. Using Western blot and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) we looked for somatic in a tract of eight deoxyguanosines (G)8 within third exon of bax in TCC and RCC cell lines and tumor specimens. However, we failed to reveal genetic alterations at least in this specific region of bax gene in urological cancers.
Conclusion: Alterations of bax, at least at investigated specific region, do not play considerable role in RCC or TCC tumorigenesis.