ArticleJapanese journal of cancer research : Gann1999
Localization of a target region of allelic loss to a 1-cM interval on chromosome 16p.13.13 in hepatocellular carcinoma.
Article in Japanese journal of cancer research : Gann, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 21 citations in OpenAlex.
- No evidence for the JAK2 (V617F) or JAK2 exon 12 mutations in primary mediastinal large B-cell lymphoma.Diagnostic molecular pathology : the American journal of surgical pathology, part B · 2009Article
- Genetics of hepatocellular tumors.Oncogene · 2006Review
- Activation of STAT3 signaling in human stomach adenocarcinoma drug-resistant cell line and its relationship with expression of vascular endothelial growth factor.World journal of gastroenterology · 2005Article
- Genetic mechanisms of hepatocarcinogenesis.Oncogene · 2002Review
- Methylation status of c-fms oncogene in HCC and its relationship with clinical pathology.World journal of gastroenterology · 2001Article
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6 authors at 2 institutions in 1 country.
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Abstract
To identify the location of the putative tumor suppressor gene on chromosome 16p that may be involved in hepatocellular carcinoma (HCC), we examined 96 primary HCCs and evaluated their patterns of allelic loss at 10 microsatellite marker loci distributed along this chromosome arm. Allelic loss at one or more loci was observed in 46 (48%) of these tumors. Through detailed deletion mapping of tumors having partial or interstitial deletions, we identified a commonly deleted region at a 1-cM interval, flanked by D16S519 and D16S3078 at 16p13.13, defining the location of a putative tumor suppressor gene for HCC. This region contains the gene for JAB (JAK-binding protein), which is responsible for negative-feedback regulation of the JAK-STAT pathway induced by cytokine stimulation, raising the possibility that inactivation of this gene may participate in hepatocarcinogenesis via genetic and/or epigenetic changes.
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