ArticleOncogene2006
Dual role of LOH at MMR loci in hereditary non-polyposis colorectal cancer?
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 29 citations in OpenAlex.
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- Functional interrogation of Lynch syndrome-associated MSH2 missense variants via CRISPR-Cas9 gene editing in human embryonic stem cells.Human mutation · 2019Article
- Sequencing of Lynch syndrome tumors reveals the importance of epigenetic alterations.Oncotarget · 2017Article
- Update on Lynch syndrome genomics.Familial cancer · 2016Review
- The onset of p53 loss of heterozygosity is differentially induced in various stem cell types and may involve the loss of either allele.Cell death and differentiation · 2014Article
- 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
- Putative precursor cancer cells in human colorectal cancer tissue.International journal of clinical and experimental pathology · 2009Article
- Tumor characteristics as an analytic tool for classifying genetic variants of uncertain clinical significance.Human mutation · 2008Article
- Refined mapping of loss of heterozygosity on 1q31.1-32.1 in sporadic colorectal carcinoma.World journal of gastroenterology · 2008Article
- Genome-wide copy neutral LOH is infrequent in familial and sporadic microsatellite unstable carcinomas.Familial cancer · 2008Article
- Mechanisms of inactivation of MLH1 in hereditary nonpolyposis colorectal carcinoma: a novel approach.Oncogene · 2007Article
- No evidence for dual role of loss of heterozygosity in hereditary non-polyposis colorectal cancer.Oncogene · 2007Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
hMLH1 and hMSH2 can be considered tumor suppressor genes, as both alleles must be inactivated in order to lose the mismatch repair (MMR) function. In this regard, it has been proposed that LOH at MMR loci is a common Knudson's second-hit mechanism in HNPCC patients. However, experimental evidence supporting this view is scarcely found in the literature. We have performed a comprehensive analysis of LOH in 45 HNPCC tumors carrying a germline alteration in MMR loci. Overall, we have detected LOH at MMR loci in 56% of the cases. However, up to 40% of the LOH events targeted the mutant allele, arguing against a second-hit role in these tumors. Interestingly, the age at diagnosis was significantly older in these patients. To explain this and previous data, we propose a dual role for LOH at MMR loci in HNPCC.
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