PMID- 11351301
OWN - NLM
STAT- MEDLINE
DCOM- 20010628
LR  - 20160303
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 92
IP  - 6
DP  - 2001 Jun 15
TI  - Assessments of clonal composition of colorectal adenomas by FISH analysis of 
      chromosomes 1, 7, 13 and 20.
PG  - 816-23
AB  - Chromosome banding analysis has shown that numerical aberrations, in particular 
      gains of chromosomes 7, 13 and 20, are common in colorectal adenomas but cannot 
      provide reliable information on the size of the abnormal clones in vivo. We 
      examined interphase nuclei from 70 colorectal adenomas, of which 64 had been 
      previously karyotyped, using fluorescence in situ hybridization (FISH) with 
      probes for the pericentromeric regions of chromosomes 1, 7, 13 and 20. Gain of 
      chromosome 7 was seen in 34% of the analyzed adenomas, +13 was seen in 44% and 
      trisomy 20 was found in 32% of the adenomas, verifying that the trisomies are in 
      vivo phenomena. The median proportion of cells with trisomy was larger than 50%. 
      A comparison with the G-banding analysis showed a good correlation between the 
      results yielded by the 2 methods. Based on the clonal size and karyotypic 
      findings, a likely order of events during clonal evolution could be ascribed to 
      each case. More than 1 numerical aberration was detected by FISH analysis in 16 
      adenomas. In 6 adenomas, a clone with only trisomy 7 was present alongside a 
      clone with additional gain(s) of chromosomes 13 and/or 20. Seven cases had gain 
      of chromosome 13 and/or gain of chromosome 20 in the largest clone, suggesting 
      that a clone with either of these changes was present before the changes in 
      chromosome 7 copy number took place. On the basis of the results of this combined 
      meta- and interphase cytogenetic study, we conclude that gains of chromosomes 7, 
      13 and 20 are common in colorectal adenomas and that the trisomies usually are 
      present in a large proportion of the cells. They seem to be primary chromosome 
      aberrations in some adenomas, whereas in others they arise secondarily as part of 
      the clonal evolution. Although the first gain usually is of chromosome 7, it is 
      evident that it is the end result of the chromosomal aberrations, not the exact 
      sequence in which they occur, that determines the pathogenetic consequences.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Bomme, L
AU  - Bomme L
AD  - Department of Medical Genetics, Odense University, University of Southern 
      Denmark, Odense, Denmark. l.bomme@ishmed.ou.dk
FAU - Lothe, R A
AU  - Lothe RA
FAU - Bardi, G
AU  - Bardi G
FAU - Fenger, C
AU  - Fenger C
FAU - Kronborg, O
AU  - Kronborg O
FAU - Heim, S
AU  - Heim S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
SB  - IM
MH  - Adenoma/*genetics
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Chromosome Aberrations
MH  - Chromosome Banding
MH  - *Chromosomes, Human, Pair 1
MH  - *Chromosomes, Human, Pair 13
MH  - *Chromosomes, Human, Pair 20
MH  - *Chromosomes, Human, Pair 7
MH  - Colorectal Neoplasms/*genetics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Karyotyping
MH  - Middle Aged
MH  - Models, Genetic
MH  - Trisomy
EDAT- 2001/05/15 10:00
MHDA- 2001/06/29 10:01
CRDT- 2001/05/15 10:00
PHST- 2001/05/15 10:00 [pubmed]
PHST- 2001/06/29 10:01 [medline]
PHST- 2001/05/15 10:00 [entrez]
AID - 10.1002/ijc.1275 [pii]
AID - 10.1002/ijc.1275 [doi]
PST - ppublish
SO  - Int J Cancer. 2001 Jun 15;92(6):816-23. doi: 10.1002/ijc.1275.