Boland C R, Sato J, Saito K, Carethers J M, Marra G, Laghi L, Chauhan D P
Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093-0688, USA.
Cancer Detect Prev. 1998;22(5):377-82. doi: 10.1046/j.1525-1500.1998.00050.x.
Our understanding of the pathogenesis of cancer has undergone a revolution over the past decade. Tumors develop by the accumulation of damage to genes that regulate cell growth. Many of the genes responsible for disregulation of cell growth have been identified, as have the processes that lead to the genetic damage. One of the most important concepts that has facilitated our understanding of carcinogenesis is that of genetic or "genomic" instability, which is required to permit a sufficient amount of genetic damage to accumulate to permit the neoplastic phenotype to emerge and evolve. Two mechanisms that lead to genomic instability--one of which involves the loss of chromosomal fragments from the nucleus, and a second which is characterized by microsatellite instability--are discussed.
