p16 is a major inactivation target in hepatocellular carcinoma

The p16INK4A gene encodes 2 cell cycle regulator proteins, p16 and p14ARF, by alternative splicing. This genetic locus also contains another cell cycle regulator gene, p15INK4B, which encodes p15. The inactivation of the p16 protein has been demonstrated in some hepatocellular carcinomas (HCCs); however, the inactivation of the other 2 cell regulator proteins and their inactivation patterns are not well characterized.

[1]  F. Imazeki,et al.  [Molecular mechanism of hepatocarcinogenesis]. , 1999, Gan to kagaku ryoho. Cancer & chemotherapy.

[2]  H. Asakura,et al.  p16INK4 is inactivated by extensive CpG methylation in human hepatocellular carcinoma , 1999 .

[3]  W. Lau,et al.  High frequency of p16INK4A gene alterations in hepatocellular carcinoma , 1999, Oncogene.

[4]  S. Clark,et al.  Loss of p16INK4 expression by methylation is associated with lifespan extension of human mammary epithelial cells. , 1998, Cancer research.

[5]  T. Sekiya,et al.  Accumulation of genetic alterations and their significance in each primary human cancer and cell line. , 1998, Mutation research.

[6]  P. Jones,et al.  The role of DNA methylation in expression of the p19/p16 locus in human bladder cancer cell lines. , 1998, Cancer research.

[7]  Z. Piao,et al.  Homozygous deletions of the CDKN2 gene and loss of heterozygosity of 9p in primary hepatocellular carcinoma. , 1998, Cancer letters.

[8]  Hoguen Kim,et al.  Allelotype analysis of hepatocellular carcinoma , 1998, International journal of cancer.

[9]  A. El‐Naggar,et al.  Methylation, a major mechanism of p16/CDKN2 gene inactivation in head and neck squamous carcinoma. , 1997, The American journal of pathology.

[10]  D. Haber,et al.  Splicing into Senescence: The Curious Case of p16 and p19ARF , 1997, Cell.

[11]  N. Nishida,et al.  Alteration of cell cycle-related genes in hepatocarcinogenesis. , 1997, Histology and histopathology.

[12]  J. Sheu.  Molecular mechanism of hepatocarcinogenesis , 1997, Journal of gastroenterology and hepatology.

[13]  Hoguen Kim,et al.  Relationship between loss of heterozygosity of tumor suppressor genes and histologic differentiation in hepatocellular carcinoma , 1997, Cancer.

[14]  M. Buendia,et al.  Comprehensive allelotyping of human hepatocellular carcinoma , 1997, Oncogene.

[15]  F. Bosman,et al.  Germ‐line mutations of the p16INK4(MTS1) gene occur in a subset of patients with hepatocellular carcinoma , 1997, Hepatology.

[16]  G. Thomas,et al.  Concerted nonsyntenic allelic losses in hyperploid hepatocellular carcinoma as determined by a high-resolution allelotype. , 1997, Cancer research.

[17]  B. Leggett,et al.  Frequency of mutation and deletion of the tumor suppressor gene CDKN2A (MTS1/p16) in hepatocellular carcinoma from an Australian population , 1997, Hepatology.

[18]  M. Miwa,et al.  Inactivation of p16/CDKN2 and p15/MTS2 genes in different histological types and clinical stages of primary ovarian tumors , 1996, International journal of cancer.

[19]  C. Sherr.  Cancer Cell Cycles , 1996, Science.

[20]  J. Herman,et al.  Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[21]  S. Hirohashi,et al.  Inactivation of p16INK4 in hepatocellular carcinoma , 1996, Hepatology.

[22]  S. Hirohashi,et al.  Inactivation of p16(INK4) in hepatocellular carcinoma , 1996 .

[23]  N. Nishida,et al.  Infrequent alterations of the p16INK4A gene in liver cancer , 1996, International journal of cancer.

[24]  T. Goodrow,et al.  Deletion and mutation analyses of the P16/MTS-1 tumor suppressor gene in human ductal pancreatic cancer reveals a higher frequency of abnormalities in tumor-derived cell lines than in primary ductal adenocarcinomas. , 1996, Cancer research.

[25]  Z. Tang,et al.  Alterations of CDKN2(p16/MTS1) exon 2 in human hepatocellular carcinoma. , 1996, Oncology reports.

[26]  F. Zindy,et al.  Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest , 1995, Cell.

[27]  J. Herman,et al.  Inactivation of the CDKN2/p16/MTS1 gene is frequently associated with aberrant DNA methylation in all common human cancers. , 1995, Cancer research.

[28]  G. Hannon,et al.  Intragenic mutations of CDKN2B and CDKN2A in primary human esophageal cancers. , 1995, Human molecular genetics.

[29]  Kathleen R. Cho,et al.  Frequency of homozygous deletion at p16/CDKN2 in primary human tumours , 1995, Nature Genetics.

[30]  C. Busch,et al.  High frequency of chromosome 9p allelic loss and CDKN2 tumor suppressor gene alterations in squamous cell carcinoma of the bladder. , 1995, Journal of the National Cancer Institute.

[31]  Y. Nakamura,et al.  Evidence for the presence of two tumour-suppressor genes for hepatocellular carcinoma on chromosome 13q. , 1995, British Journal of Cancer.

[32]  K. Yeo,et al.  Characterization of cell lines established from human hepatocellular carcinoma , 1995, International journal of cancer.

[33]  S. Tavtigian,et al.  Complex structure and regulation of the P16 (MTS1) locus. , 1995, Cancer research.

[34]  C. D. Edwards,et al.  A novel p16INK4A transcript. , 1995, Cancer research.

[35]  J. Jiricny,et al.  GTBP, a 160-kilodalton protein essential for mismatch-binding activity in human cells. , 1995, Science.

[36]  A. Okamoto,et al.  Mutations and altered expression of p16INK4 in human cancer. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[37]  Gregory J. Hannon,et al.  pl5INK4B is a potentia| effector of TGF-β-induced cell cycle arrest , 1994, Nature.

[38]  B. Vogelstein,et al.  Purification of DNA from formaldehyde fixed and paraffin embedded human tissue. , 1985, Biochemical and biophysical research communications.

[39]  H. Edmondson,et al.  Primary carcinoma of the liver. A study of 100 cases among 48,900 necropsies , 1954, Cancer.

[40]  W. Lau,et al.  Detection of aberrant p16 methylation in the plasma and serum of liver cancer patients. , 1999, Cancer research.

[41]  J. Yokota,et al.  Inactivation of p16 in Hepatocellular Carcinoma , 1998 .

[42]  D. Louis,et al.  CDKN2/p16 or RB alterations occur in the majority of glioblastomas and are inversely correlated. , 1996, Cancer research.

[43]  G. Peters,et al.  Genetic alterations of cyclins, cyclin-dependent kinases, and Cdk inhibitors in human cancer. , 1996, Advances in cancer research.

[44]  T. Ishikawa,et al.  Allelotype study of primary hepatocellular carcinoma. , 1991, Cancer research.

[45]  A. Okamoto,et al.  Mutations and altered expression of p 16 INK 4 in human cancer ( p 53 protein / tumor-suppressor gene / cyclin Di / retinoblastoma protein ) , 2022 .