ArticleOncogene2007
No evidence for dual role of loss of heterozygosity in hereditary non-polyposis colorectal cancer.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Gene variants of unknown clinical significance in Lynch syndrome. An introduction for clinicians.Familial cancer · 2013Article
- Article
- Unbalanced replication as a major source of genetic instability in cancer cells.American journal of blood research · 2012Article
- MYH biallelic mutation can inactivate the two genetic pathways of colorectal cancer by APC or MLH1 transversions.Familial cancer · 2010Article
- Ultradeep sequencing of a human ultraconserved region reveals somatic and constitutional genomic instability.PLoS biology · 2010Article
- Partial loss of heterozygosity events at the mutated gene in tumors from MLH1/MSH2 large genomic rearrangement carriers.BMC cancer · 2009Article
- Promoter methylation in the genesis of gastrointestinal cancer.Yonsei medical journal · 2009Review
- Tumor characteristics as an analytic tool for classifying genetic variants of uncertain clinical significance.Human mutation · 2008Article
- Genome-wide copy neutral LOH is infrequent in familial and sporadic microsatellite unstable carcinomas.Familial cancer · 2008Article
- Epigenetic Loss of MLH1 Expression in Normal Human Hematopoietic Stem Cell Clones is Defined by the Promoter CpG Methylation Pattern Observed by High-Throughput Methylation Specific Sequencing.International journal of stem cell research and therapyArticle
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hereditary non-polyposis colorectal cancer (HNPCC) is caused by germline mutations in mismatch repair (MMR) genes, mostly MLH1 and MSH2. Somatic inactivation of the wild-type allele of the respective MMR gene is required for tumor development. Unexpectedly, a recent study utilizing DNA from paraffin-embedded tissue material detected frequent loss of the mutant MMR gene allele in HNPCC tumors. Dual role for loss of heterozygosity (LOH) was proposed. If somatic loss of the wild-type MMR gene allele had occurred through point mutation or promoter hypermethylation, frequent somatic deletions at the region of the MMR gene locus, perhaps targeting other relevant cancer genes, could quite commonly lead to loss of the mutant allele. To test this hypothesis, we studied a population-based series of 25 fresh-frozen HNPCC tumors with a germline mutation in MLH1 or MSH2 for LOH. Fourteen of the 25 tumors (56%) showed LOH at the respective locus, and all 14 losses targeted the wild-type allele (P=0.00006). These results strongly support the traditional two-hit model of HNPCC gene inactivation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.