S. PoeaimB. RerkamnuaychokeS. JesdapatarakulA. CampiranonKing Mongkut's Institute of Technology LadkrabangMahidol UniversityVajira HospitalKasetsart University2018-06-212018-06-212005-07-15Cancer Genetics and Cytogenetics. Vol.160, No.2 (2005), 152-159016546082-s2.0-21344467201https://repository.li.mahidol.ac.th/handle/20.500.14594/16314Much information has been reported on the genetic and genomic alterations in colorectal cancer (CRC) in various countries; however, nonrandom chromosomal alterations in Thai patients have not been described. As a first step toward understanding the underlying genetic changes and determining early chromosomal changes of tumor development in this population, we used comparative genomic hybridization (CGH) to screen for losses and gains of DNA sequences along chromosomes in 20 morphologically normal tumor surroundings (MNTS) and 40 CRC tissues from 40 patients. In CRC, we detected gains of chromosome arms 20q (60%), 8q (25%), 19q (22.5%), and 19p (20%), as well as losses of chromosome arms 18q (25%) and 4q (20%). There were no differences in genetic alteration between colon and rectal cancer. In morphologically normal tumor surroundings (MNTS) tissues, gains on 19p and 19q were most frequent. We suggest that gains of this chromosome are early events in the progression of CRC, followed by gains on 8q and 20q and losses on 4q and 18q at later stages. Based on our cytogenetic data by comparison of 2 tissue groups in the same cases, we discuss the monoclonal model followed by lateral epithelial spread as an explanation of multiple CRC. Identification and characterization of the causative genes for these cancer syndromes have enabled precise pre-symptomatic detection of mutations in individuals who bear a prior risk of developing CRC. © 2005 Elsevier Inc. All rights reserved.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyArticleSCOPUS10.1016/j.cancergencyto.2004.12.011