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The frequency of biallelic inactivations of the MYH locus described in these studies appears to be so high that mutations in the MYH gene might turn out to be the principal cause of this syndrome.Conclusions MMR defects were the rst DNA repair malfunction to be linked with colon cancer.More recently, inactivation of MBD, MYH and MGMT, either through mutations or through transcriptional silencing, has also been implicated in this malignancy.A detailed study of these interactions is likely to lead to a better understanding of the transformation process of the colonic epithelium.In the followup study to, the authors identied seven further unrelated patients with colorectal adenomas with biallelic germline displayed a signicant excess of somatic G:C T:A mutations in the mutations in MYH.The colorectal tumours from affected individuals APC gene.These ndings conrm the role of MYH in colorectal adenoma and carcinoma predisposition.These studies showed that the enzyme consisted of two domains, methylated DNA binding domain and an endonuclease domain, both of which are functional.Describes the identication of the hMLH gene and shows that   its polypeptide product interacts with hMLH and that its overexpression interferes with MMR.Demonstration of the requirement for EXO in human cellfree MMR.The authors describe the identication of an HNPCC patient who appeared to be free of mutations in the MMR genes.However, one allele of hMLH was shown to be silenced by methylation in his lymphocytes, and the tumor appeared to have lost the wild type hMLH allele.Shows that oxoguanine incorporated into DNA during DNA replication is removed by the MMR system.These levels are high in cells lacking MTH, which detoxies the oxidized nucleotide pool, but the authors show that the MMR system is involved in this repair process also in cells expressing MTH.Scharer OD, Jiricny J: Recent progress in the biology, chemistry and structural biology of DNA glycosylases. Boldogh I, Milligan D, Lee MS, Bassett H, Lloyd RS, McCullough AK: hMYH cell cycledependent expression, subcellular localization and association with replication foci: evidence suggesting replication coupled repair of adenine: oxoguanine mispairs. Gu Y, Parker A, Wilson TM, Bai H, Chang DY, Lu AL: Human MutY homolog, a DNA glycosylase involved in base excision repair, physically and functionally interacts with mismatch repair proteins human MutS <a href="https://www.ncbi.nlm.nih.gov/pubmed/11562962">buy Tenofovir alafenamide</a> homolog human MutS homolog. Gayet J, Zhou XP, Duval A, Rolland S, Hoang JM, Cottu P, Hamelin R: Extensive characterization of genetic alterations in a series of human colorectal cancer cell lines. Rowan AJ, Lamlum H, Ilyas M, Wheeler J, Straub J, Papadopoulou A, Bicknell D, Bodmer WF, Tomlinson IP: APC mutations in sporadic colorectal tumors: a mutational hotspot and interdependence of the two hits.Oncogene. Cell. Cancer Res. Nat Genet. Cell. Cancer Res. Genes Dev. Nat Genet. Nat Genet. Cell. Proc Natl Acad Sci USA. Cancer Res. Cell. Oncogene. Cancer Res. Cancer Res. Genes Chromosomes Cancer. Nat Genet. Nat Genet. Cancer Res. www.currentopinion.com Current Opinion in Genetics Development: The user has requested enhancement of the downloaded file.View publication stats View publication stats The user has requested enhancement of the downloaded file. Nature Publishing Group View publication stats View publication stats Nature Publishing Group

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