Abstract

Loss of function of tumor suppressor genes is a condition necessary for the development of colorectal cancer (CRC). Deletions of the long arm of chromosome 18 are present in approximately 70% of CRCs, and this site contains several genes that regulate cellular functions implicated in tumorigenesis, including cell migration, proliferation, and differentiation. Recently, genome-wide association studies also showed a relationship between specific loci on 18q and risk of developing CRC. The presence of 18q loss in tumors has also been associated with poor outcome following CRC treatment. However, despite the more than 20 years since its identification in CRC, we still lack an adequate understanding of the clinical significance of 18q loss. This review details the existing data on the relationship between tumor 18q loss of heterozygosity (18qLOH) and treatment outcome for patients with CRC.

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