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Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Article DOI: 10.3791/1931-v • 28:16 min • July 28th, 2010
July 28th, 2010 •
1, 1, 1, 1, 1, 1, 2,3, 1,4, 3, 5, 5, 5, 1
1Department of Cell Biology and Anatomy, College of Medicine, University of Arizona, Tucson, 2Southern Arizona Veterans Affairs Health Care System, Tucson, AZ, 3Department of Surgery, College of Medicine, University of Arizona, Tucson, 4Biomedical Diagnostics and Research, Tucson, AZ, 5Department of Medicine, College of Medicine, University of Arizona, Tucson

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Reduced/absent expression of Pms2 and/or ERCC1 in entire crypts is a frequent event within 10 cm on each side of colonic adenocarcinomas, likely the basis of a field defect with high mutability and progression to cancer. Deficiency in Ku86 or CcOI is much less frequent in these field defects.

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Deficient Pms2 Deficient ERCC1 Deficient Ku86 Deficient CcOI Field Defect Colon Cancer Carcinogenesis Molecular Abnormalities Histologically Normal Tissue Colonic Adenocarcinoma Adenoma With Advanced Neoplasia Immunohistochemistry DNA Repair Proteins Apoptosis DNA Mismatch Repair DNA Nucleotide Excision Repair Apoptosis Resistance Mutability Progression To Colon Cancer DNA Non-homologous End Joining Cytochrome C Oxidase Subunit
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