Concurrent hypermethylation of multiple tumor‐related genes in gastric carcinoma and adjacent normal tissues

Transcriptional silencing by CpG‐island hypermethylation now is believed to be an important mechanism of tumorigenesis. To date, studies on CpG‐island hypermethylation in gastric carcinoma and adjacent normal tissues are few.

[1]  G. Kang,et al.  Correlation of p16 Hypermethylation with p16 Protein Loss in Sporadic Gastric Carcinomas , 2000, Laboratory Investigation.

[2]  R H Hruban,et al.  Hypermethylation of multiple genes in pancreatic adenocarcinoma. , 2000, Cancer research.

[3]  D. Graham,et al.  Microsatellite instability in gastric intestinal metaplasia in patients with and without gastric cancer. , 2000, The American journal of pathology.

[4]  S. Baylin,et al.  Aberrant methylation in gastric cancer associated with the CpG island methylator phenotype. , 1999, Cancer research.

[5]  M. Toyota,et al.  Distinct methylation pattern and microsatellite instability in sporadic gastric cancer , 1999, International journal of cancer.

[6]  D. Graham,et al.  Marked differences in the frequency of microsatellite instability in gastric cancer from different countries , 1999, American Journal of Gastroenterology.

[7]  S. Clark,et al.  Concurrent DNA hypermethylation of multiple genes in acute myeloid leukemia. , 1999, Cancer research.

[8]  J. Herman,et al.  CpG island methylator phenotype in colorectal cancer. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[9]  G. Kang,et al.  Correlation of methylation of the hMLH1 promoter with lack of expression of hMLH1 in sporadic gastric carcinomas with replication error. , 1999, Laboratory investigation; a journal of technical methods and pathology.

[10]  Teruhiko Yoshida,et al.  Gastric cancers of the microsatellite mutator phenotype display characteristic genetic and clinical features. , 1999, Gastroenterology.

[11]  J. Palazzo,et al.  MLH1 promoter methylation and gene silencing is the primary cause of microsatellite instability in sporadic endometrial cancers. , 1999, Human molecular genetics.

[12]  J. Herman,et al.  Hypermethylation of the hMLH1 gene promoter in human gastric cancers with microsatellite instability. , 1999, Cancer research.

[13]  Peter A. Jones,et al.  Cancer-epigenetics comes of age , 1999, Nature Genetics.

[14]  A. Jemal,et al.  Global cancer statistics , 2011, CA: a cancer journal for clinicians.

[15]  S. Leung,et al.  hMLH1 promoter methylation and lack of hMLH1 expression in sporadic gastric carcinomas with high-frequency microsatellite instability. , 1999, Cancer research.

[16]  J. Herman,et al.  Inactivation of glutathione S-transferase P1 gene by promoter hypermethylation in human neoplasia. , 1998, Cancer research.

[17]  L. Kasturi,et al.  Biallelic inactivation of hMLH1 by epigenetic gene silencing, a novel mechanism causing human MSI cancers. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[18]  J. Herman,et al.  Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[19]  R. Hunt,et al.  Meta-analysis of the relationship between Helicobacter pylori seropositivity and gastric cancer. , 1998, Gastroenterology.

[20]  J. Herman,et al.  Alterations in DNA methylation: a fundamental aspect of neoplasia. , 1998, Advances in cancer research.

[21]  Y. Bang,et al.  Alterations of p16INK4A and p15INK4B genes in gastric carcinomas , 1997, Cancer.

[22]  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.

[23]  E. Fontham,et al.  Inducible nitric oxide synthase, nitrotyrosine, and apoptosis in Helicobacter pylori gastritis: effect of antibiotics and antioxidants. , 1996, Cancer research.

[24]  J. Herman,et al.  Hypermethylation-associated inactivation indicates a tumor suppressor role for p15INK4B. , 1996, Cancer research.

[25]  S. Hirohashi,et al.  Silencing of the E-cadherin invasion-suppressor gene by CpG methylation in human carcinomas. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[26]  J. Brooks,et al.  Cytidine methylation of regulatory sequences near the pi-class glutathione S-transferase gene accompanies human prostatic carcinogenesis. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[27]  J. Herman,et al.  Silencing of the VHL tumor-suppressor gene by DNA methylation in renal carcinoma. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[28]  H. Yamasaki,et al.  Alterations of (CA)n DNA repeats and tumor suppressor genes in human gastric cancer. , 1994, Cancer research.

[29]  L. Serra-Majem,et al.  Nutrient intake and gastric cancer risk: a case-control study in Spain. , 1993, International journal of epidemiology.

[30]  S Ichii,et al.  The APC gene, responsible for familial adenomatous polyposis, is mutated in human gastric cancer. , 1992, Cancer research.

[31]  J. Minna,et al.  Occurrence of p53 gene abnormalities in gastric carcinoma tumors and cell lines. , 1991, Journal of the National Cancer Institute.

[32]  J. Guillem,et al.  Rapid detection of ras oncogenes in human tumors: applications to colon, esophageal, and gastric cancer. , 1989, Oncogene.