Abstract

Abstract A critical link exists between genomic instability and cancer development. This instability can manifest as small changes at the nucleotide level or as gross chromosomal alterations. Mutations in the genes that encode DNA damage response proteins are responsible for a variety of genomic instability syndromes including Hereditary Non-Polyposis Colorectal Carcinoma, Bloom syndrome, Ataxia-telangiectasia, BRCA1 and BRCA2 mutated breast and ovarian cancers and Fanconi anaemia. Similarly epigenetic silencing of genes associated with the maintenance of genomic stability have also been implicated in the pathogenesis of cancer. Here, I discuss how different tumours may be classified not only by tumour site but also by the type of underlying genetic instability. This type of classification may assist in the optimization of treatment regimens as well as informing the development of new therapeutic approaches in particular based on “synthetic lethality”. I will illustrate these principles by demonstrating potential “synthetic lethal” treatments for mismatch repair deficient cancers. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr AACR1-1.

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