THE CHROMOSOMAL INSTABILITY PATHWAY IN COLON CANCER

By M. Pino, D. Chung. Gastroenterology, 2010

900 citations recorded by the source corpus.

The acquisition of genomic instability is a crucial feature in tumor development and there are at least 3 distinct pathways in colorectal cancer pathogenesis: the chromosomal instability (CIN), microsatellite instability (MSI), and CpG island methylator phenotype (CIMP) pathways. Most cases of colorectal cancer arise through the CIN pathway, which is characterized by widespread imbalances in chromosome number (aneuploidy) and loss of heterozygosity (LOH). It can result from defects in chromosomal segregation, telomere stability, and the DNA damage response, although the full complement of genes underlying CIN remains incompletely described. Coupled with the karyotypic abnormalities observed in CIN tumors are the accumulation of a characteristic set of mutations in specific tumor suppressor genes and oncogenes that activate pathways critical for colorectal cancer initiation and progression. Whether CIN creates the appropriate milieu for the accumulation of these mutations or vice versa remains a provocative and unanswered question. The goal of this review is to provide an updated perspective on the mechanisms that lead to CIN and the key mutations that are acquired in this pathway.

Subfields: Cancer Research, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/6fa30912fa1b9ec3ca167e720765d71258f58f00

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Citations in the corpus

• Colorectal Carcinoma: A General Overview and Future Perspectives in Colorectal Cancer (2017, background): “Finally, loss-of-function mutations in TP53, which encodes for p53, the main cell-cycle checkpoint, cause an uncontrolled entry in the cell cycle [27].”