title: Allelic losses of 17p, 5q, and 18q loci in diploid and aneuploid populations of multiploid colorectal carcinomas.
abstract: 17p, 5q, and 18q allelic losses are involved in the pathogenesis and progression of colorectal carcinoma, and DNA aneuploidy in this type of cancer is thought to result from alterations of these chromosomal loci. However, genetic differences between diploid and aneuploid populations of multiploid carcinoma, defined as the coexistence of diploid and aneuploid populations in the same area, remain unclear. The differences in 17p, 5q, and 18q allelic losses between the diploid and aneuploid populations in 24 sporadic DNA multiploid colorectal carcinomas were analyzed by use of crypt isolation coupled with DNA cytometric sorting and polymerase chain reaction assay. 17p Allelic loss was observed in 7 of 22 diploid populations excluding 1 case of microsatellite instability but was found in 21 of 23 aneuploid populations. Although 5q allelic loss was detected in only 3 of 22 diploid populations, 13 of 22 aneuploid populations had 5q allelic loss. Losses of the 18q allele were frequently found in aneuploid populations (15 of 20), although no 18q allelic loss was detected in corresponding diploid populations. 17p Allelic losses may play an important role in the progression from a diploid status to an aneuploid status in a specific subset of colorectal cancer. However, 18q or 5q allelic losses do not appear to precede nor to facilitate the aneuploid clonal divergence of cancer cells. Multiploidy is a useful model to study genetic alterations between diploid and aneuploid populations.
authors.affiliation: Department of First Internal Medicine, School of Medicine, Iwate Medical University, Morioka, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Sugai
authors.forename: W
authors.initials: W
authors.lastname: Habano
authors.forename: S
authors.initials: S
authors.lastname: Nakamura
authors.forename: H
authors.initials: H
authors.lastname: Sato
authors.forename: N
authors.initials: N
authors.lastname: Uesugi
authors.forename: S
authors.initials: S
authors.lastname: Orii
authors.forename: C
authors.initials: C
authors.lastname: Itoh
authors.forename: R
authors.initials: R
authors.lastname: Katoh
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000782:Aneuploidy; D002886:Chromosomes, Human, Pair 17 / Q000235:genetics*; D002887:Chromosomes, Human, Pair 18 / Q000235:genetics*; D002895:Chromosomes, Human, Pair 5 / Q000235:genetics*; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000473:pathology; D004273:DNA, Neoplasm / Q000235:genetics; D004171:Diploidy; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D019656:Loss of Heterozygosity; D008297:Male; D008875:Middle Aged; D016159:Tumor Suppressor Protein p53 / Q000235:genetics
chemical_list: D004273:DNA, Neoplasm; D016159:Tumor Suppressor Protein p53