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Infrequent alterations of the p16 INK4A gene in liver cancer
Author(s) -
Kita Ryuichi,
Nishida Naoshi,
Fukuda Yoshihiro,
Azechi Hidemasa,
Matsuoka Yoko,
Komeda Toshiki,
Sando Takehiro,
Nakao Kazuwa,
Ishizaki Kanji
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19960717)67:2<176::aid-ijc4>3.0.co;2-q
Subject(s) - liver cancer , gene , medicine , biology , cancer , pathology , genetics , cancer research , oncology
We examined the genomic status of the p16 INK4A (inhibitor of cyclin‐dependent kinase 4 A) and cyclin‐dependent kinase 4 ( CDK 4) genes in 62 human hepatocellular carcinomas (HCCs), 5 cholangiocellular carcinomas and 6 cell lines derived from human liver cancers. Although no samples showed the homozygous deletion of the p16 INK4A gene, we detected intragenic mutations of the p16 INK4A gene in 3 HCCs and one HCC cell line, which led to an amino‐acid substitution or a frameshift. In 2 HCC samples with mis‐sense mutations of the p16 INK4A gene, loss of heterozygosity on 9p22 was also detected, suggesting that the loss of function of p16 was induced during hepatocarcinogenesis. On the other hand, amplification or rearrangement of the CDK 4 gene was not detected in any samples examined in this study. These results indicated that the mutations or deletions of the p16 INK4A gene are not frequent, but may play a role in a sub‐set of human HCC. © 1996 Wiley‐Liss, Inc.