ArticleProceedings of the National Academy of Sciences of the United States of America1989
Loss of heterozygosity suggests tumor suppressor gene responsible for primary hepatocellular carcinoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 186 citations in OpenAlex.
- Chromosome alterations in human hepatocellular carcinomas correlate with aetiology and histological grade--results of an explorative CGH meta-analysis.British journal of cancer · 2005Pooled it
- Preemptive Homology-Directed DNA Repair Fosters Complex Genomic Rearrangements in Hepatocellular Carcinoma.Translational oncology · 2020Article
- Nm23-H1 inhibits lung cancer bone-specific metastasis by upregulating miR-660-5p targeted SMARCA5.Thoracic cancer · 2020Article
- Overexpression of SMARCA5 correlates with cell proliferation and migration in breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- The cooperative effect of p53 and Rb in local nanotherapy in a rabbit VX2 model of hepatocellular carcinoma.International journal of nanomedicine · 2013Article
- Article
- Developmental context determines latency of MYC-induced tumorigenesis.PLoS biology · 2004Article
- Aberrant caspase-activated DNase (CAD) transcripts in human hepatoma cells.British journal of cancer · 2003Article
- Functional evidence for a squamous cell carcinoma mortality gene(s) on human chromosome 4.Oncogene · 2002Article
- Frequent genomic imbalances suggest commonly altered tumour genes in human hepatocarcinogenesis.British journal of cancer · 2001Article
- Loss of heterozygosity at 4p16.3 and mutation of FGFR3 in transitional cell carcinoma.Oncogene · 2001Article
- Localized hepatocellular carcinoma: therapeutic options.Current gastroenterology reports · 2000Review
- Localization of a target region of allelic loss to a 1-cM interval on chromosome 16p.13.13 in hepatocellular carcinoma.Japanese journal of cancer research : Gann · 1999Article
- Chromosomal aberrations in human hepatocellular carcinomas associated with hepatitis C virus infection detected by comparative genomic hybridization.British journal of cancer · 1999Article
- Loss of heterozygosity and microsatellite instability in hepatocellular carcinoma in Taiwan.British journal of cancer · 1999Article
- Nonrandom cytogenetic alterations in hepatocellular carcinoma from transgenic mice overexpressing c-Myc and transforming growth factor-alpha in the liver.The American journal of pathology · 1999Article
- PTEN/MMAC1 mutations in hepatocellular carcinomas: somatic inactivation of both alleles in tumors.Japanese journal of cancer research : Gann · 1999Article
- Genetic alterations in hepatocellular carcinomas: association between loss of chromosome 4q and p53 gene mutations.British journal of cancer · 1999Article
- Absence of mutation of the p73 gene localized at chromosome 1p36.3 in hepatocellular carcinoma.British journal of cancer · 1999Article
- Diminished expression of phosphatidylethanolamine N-methyltransferase 2 during hepatocarcinogenesis.The Biochemical journal · 1999Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Primary hepatocellular carcinoma (PHC), epidemiologically associated with chronic hepatitis B virus (HBV) infection, has historically been felt to be caused by the activation or introduction of an oncogene. However, transforming sequences from human PHC have not been reproducibly isolated. In this paper, evidence is presented that suggests PHC may result instead from the loss of an anti-oncogene. Seven of 12 human primary liver tumors tested against a panel of restriction fragment length polymorphisms (RFLPs) demonstrated loss of constitutional heterozygosity for markers on chromosome 4. Tumor and nontumor liver tissue were typed for 11 chromosome 4 RFLPs. In addition, at least one RFLP on nine other chromosomes (1, 2, 6, 7, 9, 11, 13, 14, and 17) was tested for allelic loss. Seven of nine tumors constitutionally heterozygous for chromosome 4q markers showed allele loss in tumor tissue. Six of the seven samples were jointly informative for both 4p and 4q markers. Five of the six demonstrated loss for only 4q RFLPs. In one individual, in which two samples were taken from distant locations within the same tumor, both samples showed loss of the same alleles. Among the other chromosomes informative for allele loss, one tumor showed changes on 13q. No other changes were observed in RFLPs located on the eight other chromosomes tested. These results indicate that an anti-oncogene may be located on 4q and suggest a mechanism for PHC and other cancers seroepidemiologically related to virus infection. Liver cancer caused by chronic HBV infection or other environmental agents may be linked through genetic events responsible for the loss of a tumor suppressor locus (anti-oncogene) located on chromosome 4.
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