Sign up for Table of Contents Alerts.
Email this page
Print this page
Extra Views
Is Base Excision Repair a Tumor Suppressor Mechanism?
Joann B. Sweasy, Tieming Lang and Daniel DiMaio
volume 5 | issue 3
1 february 2006Pages: 250 - 259
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.
Epidemiologic studies have long implied that the emergence of cancer requires the accumulation of multiple genetic changes, and molecular genetic studies have established that discrete mutations in oncogenes and tumor suppressor genes can contribute to carcinogenesis The discovery that hereditary non-polyposis colon carcinoma (HNPCC) is ultimately due to mutations that affect DNA mismatch repair provides direct evidence that impaired DNA repair can result in tumorigenesis, presumably by inducing carcinogenic mutations in growth regulatory genes. We suggest that mutations that impair the base excision repair (BER) pathway and indeed polymorphisms in genes encoding BER proteins may increase the probability of developing cancer by inducing mutagenesis. Here, we review the evidence that mutations and polymorphisms in one of the major cellular DNA repair pathways, BER, can influence cancer risk in humans.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.