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Aberrant crypt foci as precursors in colorectal cancer progression
Author(s) -
Orlando Frank A.,
Tan Dongfeng,
Baltodano Juan D.,
Khoury Thaer,
Gibbs John F.,
Hassid Victor J.,
Ahmed Bestoun H.,
Alrawi Sadir J.
Publication year - 2008
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21106
Subject(s) - colorectal cancer , loss of heterozygosity , aberrant crypt foci , genome instability , epigenetics , phenotype , medicine , microsatellite instability , cancer research , pathology , population , cancer , chromosome instability , crypt , oncology , biology , genetics , gene , colonic disease , dna , dna damage , allele , environmental health , microsatellite , chromosome
Colorectal cancer progression originates when accumulated genetic and epigenetic alterations cause genomic instability and a malignant phenotype. Subsequent molecular pathway deregulation leads to histopathologic changes that are clinically evident as aberrant crypt foci (ACF) and visualized by high‐magnification chromoscopic colonoscopy. ACF are biomarkers of increased colorectal cancer risk, particularly those with dysplastic features. Genetic profiling using genomic instability, loss of heterozygosity, and methylation analysis has revealed a minority population of ACF genotypically analogous to cancer. J. Surg. Oncol. 2008;98:207–213. © 2008 Wiley‐Liss, Inc.