Chromosomal 20q gain in the DNA diploid component of aneuploid colorectal carcinomas.
The order of appearance of different genetic aberrations during the shift from diploidy/near-diploidy to aneuploidy in colorectal cancers is not yet clear. We studied genetic alterations in flow cytometrically-sorted DNA diploid and corresponding aneuploid epithelial cell populations from each of 20 colorectal tumors using comparative genomic hybridization, FISH, and PCR. Analysis of the 19 cases in which aberrations were found in the flow-sorted diploid population indicated that large-scale aneuploidization in colorectal cancer was preceded by amplification of oncogene(s) localized to chromosome 20q13.2 and by KRAS mutations, but not by TP53 deletions or losses of large chromosomal regions such as 4q, 8p and 18q.
De Angelis
Paula M
PM
The Pathology Clinic, University of Oslo, Rikshospitalet-Radiumhospitalet Medical Center, 0027 Oslo, Norway. p.d.angelis@medisin.uio.no
Stokke
Trond
T
Beigi
Marzieh
M
Flatberg
Gøril
G
Enger
Marianne
M
Haug
Kristiane
K
Aass
Hans Christian D
HC
Schjølberg
Aasa
A
Andresen
Per Arne
PA
Ariansen
Sarah
S
Bø
Anne Signe
AS
Mjåland
Odd
O
Clausen
Ole Petter
OP
D000782:Aneuploidy; D002471:Cell Transformation, Neoplastic / Q000235:genetics; D002869:Chromosome Aberrations; D002890:Chromosomes, Human, Pair 20 / Q000235:genetics*; D015179:Colorectal Neoplasms / Q000235:genetics / Q000473:pathology*; D004252:DNA Mutational Analysis; D004171:Diploidy; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology; D005434:Flow Cytometry; D011905:Genes, ras / Q000235:genetics; D015894:Genome, Human; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D019656:Loss of Heterozygosity; D009154:Mutation; D009693:Nucleic Acid Hybridization / Q000379:methods; D016159:Tumor Suppressor Protein p53 / Q000235:genetics
D016159:Tumor Suppressor Protein p53