Lack of frameshift mutations at coding mononucleotide repeats in hepatocellular carcinoma in Japanese patients

Autor: Yuji Matsuzawa, Iwao Yabuuchi, Yasuo Matsuda, Nobuyuki Ito, Shinji Tamura, Sumio Kawata, Ayuko Saeki, Shinichi Kiso
Rok vydání: 2000
Předmět:
Zdroj: Cancer. 88:1025-1029
ISSN: 1097-0142
0008-543X
DOI: 10.1002/(sici)1097-0142(20000301)88:5<1025::aid-cncr11>3.0.co;2-u
Popis: BACKGROUND Microsatellite instability occurs frequently in hereditary nonpolyposis colorectal carcinoma, in sporadic gastrointestinal carcinoma, and in other tumors. In these tumors, slippage-related frameshift mutations have been detected at coding mononucleotide repeats in genes such as those for transforming growth factor-β receptor type II (TGFβRII), mannose 6-phosphate/insulinlike growth factor II receptor (M6P/IGFIIR), hMSH3, hMSH6, and Bcl-2–associated X protein (BAX). Because these genes regulate cell growth or repair DNA mismatches, loss of their function is thought to promote tumor development. The authors screened for these frameshift mutations and investigated the incidence of microsatellite instability (MI) in hepatocellular carcinoma (HCC) in Japan. METHODS Fifty HCC samples were analyzed in this study. The authors used polymerase chain reactions to screen for frameshift mutation at the TGFβRII (A)10 tract, the M6P/IGFIIR (G)8 tract, the hMSH3 (A)8 tract, the hMSH6 (C)8 tract, and the BAX (G)8 tract. For MI analysis, matched tumor and nontumor liver DNA were investigated with respect to 10 microsatellite loci. RESULTS No frameshift mutation was detected in any case, and only 4% of these cancers exhibited MI in comparisons between tumor and nontumor liver specimens. CONCLUSIONS This study suggests that frameshift mutation at coding mononucleotide repeats within TGFβRII, M6P/IGFIIR, hMSH3, hMSH6, and BAX genes did not seem to be involved in hepatocarcinogenesis in the Japanese population studied. Cancer 2000;88:1025–9. © 2000 American Cancer Society.
Databáze: OpenAIRE
Externí odkaz: