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dc.contributor.authorMao, X
dc.contributor.authorHamoudi, RA
dc.contributor.authorTalbot, IC
dc.contributor.authorBaudis, M
dc.identifier.citationCANCER GENETICS AND CYTOGENETICS, 2006, 167 pp. 1 - 14
dc.description.abstractColorectal cancer (CRC) remains a significant public health challenge despite our increased understanding of the genetic defects underlying the pathogenesis of this common disease. It has been thought that multiple mechanisms lead to the malignant phenotype, with familial predisposition syndromes accounting for only a small proportion of all CRC cases. To identify additional loci likely involved in CRC and to test the hypothesis of allele-specific loss of heterozygosity (LOH) for the localization of CRC susceptibility genes, we initially conducted a genome-wide allelotyping analysis of 48 adenomas from a patient with familial adenomatous polyposis coli (FAP) and 63 adenomas from 7 patients with sporadic CRC using 79 fluorescently tagged oligonucleotide primers amplifying microsatellite loci covering the human genome. Frequent allelic losses were identified at D17S802 (41%) D7S518 (40%), D18S53 (38%), D10S249 (32%), D2S391 (29%), D16S419 (27%), D15S1005 and D15S120 (24%), D9S274 and D11S1318 (23%), D14S65 (20%), D14S274 and D17S953 (19%), D19S424 (18%), D5S346 and D1S397 (15%), and D6S468 (13%) in multiple FAP adenomas. Common LOH was also detected at D4S1584 (42%), D11S968 (31%), D17S953 (28%). D5S394, D9S286 and D10S249 (24%), D8S511 (23%), D13S158 (21%), D7S669 (20%), D18S58 (19%), D2S162 and D16S432 (16%), D2S206 (15%), D7S496 and D17S946 (14%), D6S292 (13%), D4S1586 and D8S283 (11%), and D1S2766 (10%) in multiple CRC adenomas. In addition, allele-specific LOH at D5S346, D15S1005, and D15S120 was observed in multiple FAP adenomas (P < 0.01) and at D2S206 and D16S423 in multiple CRC (P < 0.05). To compare Our data to previous reports, we determined the band-specific frequency of chromosomal imbalances in CRC karyotypes reported in the Mitelman database, and from the CGH results of cases accessible through the PROGENETIX website. Furthermore, published genome-wide allelotyping analysis of CRC and other allele-specific LOH studies were compiled and collated with our LOH data. The combined results not only provide a comprehensive view of genetic losses in CRC, indicating the comparability of these different techniques, but they also reveal different novel loci in multiple adenomas from FAP and sporadic CRC patients, suggesting that they represent a distinct subtype of CRC in terms of allelic losses. Allele-specific LOH is an alternative approach for cancer gene mapping. (c) 2006 Elsevier Inc. All rights reserved.
dc.format.extent1 - 14
dc.titleAllele-specific loss of heterozygosity in multiple colorectal adenomas: toward an integrated molecular cytogenetic map II
dc.typeJournal Article
rioxxterms.typeJournal Article/Review
pubs.notesaffiliation: Mao, X (Reprint Author), St Thomas Hosp, St Johns Inst Dermatol, Skin Tumour Unit, 4th Floor,S Wing,Block 7,Lambeth Palace Rd, London SE1 7EH, England. St Thomas Hosp, St Johns Inst Dermatol, Skin Tumour Unit, London SE1 7EH, England. Inst Canc Res, Canc Gene Cloning Ctr, Haddow Labs, Sutton SM2 5NG, Surrey, England. St Marks & Northwick Pk NHS Trust, Acad Dept Pathol, Harrow HA1 3UJ, Middx, England. Univ Florida, Dept Pediat, Div Hematol Oncol, Gainesville, FL 32610 USA. keywords-plus: TUMOR-SUPPRESSOR GENE; COMPARATIVE GENOMIC HYBRIDIZATION; NONPOLYPOSIS COLON-CANCER; POLYMERASE-CHAIN-REACTION; PEUTZ-JEGHERS-SYNDROME; DNA MISMATCH REPAIR; CELL-LINES; CHROMOSOME 16Q12-Q13; SEZARY-SYNDROME; FAMILY HISTORY research-areas: Oncology; Genetics & Heredity web-of-science-categories: Oncology; Genetics & Heredity author-email: [email protected] researcherid-numbers: Baudis, Michael/J-4602-2012 orcid-numbers: Baudis, Michael/0000-0002-9903-4248 number-of-cited-references: 114 times-cited: 16 usage-count-last-180-days: 0 usage-count-since-2013: 1 journal-iso: Cancer Genet. Cytogenet. doc-delivery-number: 045UI unique-id: ISI:000237767600001 da: 2018-09-04
pubs.notesNot known
pubs.embargo.termsNot known
dc.contributor.icrauthorHamoudi, Rifaten

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