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

✍ Scribed by Ayuko Saeki; Shinji Tamura; Nobuyuki Ito; Shinichi Kiso; Yasuo Matsuda; Iwao Yabuuchi; Sumio Kawata; Yuji Matsuzawa


Publisher
John Wiley and Sons
Year
2000
Tongue
English
Weight
92 KB
Volume
88
Category
Article
ISSN
0008-543X

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✦ Synopsis


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-beta receptor type ii (tgfbetarii), 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 tgfbetarii (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 tgfbetarii, m6p/igfiir, hmsh3, hmsh6, and bax genes did not seem to be involved in hepatocarcinogenesis in the japanese population studied.


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