Chromosome aberrations in adenomas of the colon. Proof of trisomy 7 in tumor cells by combined interphase cytogenetics and immunocytochemistry

Herbergs, Jos; Bruïne, Adriaan P. de; Marx, Patrick; Vallinga, M.; Stockbrügger, R.W.; Ramaekers, Frans C.S.; Arends, Jan Willem; Hopman, Anton H. N.

doi:10.1002/ijc.2910570604

Cited by 34 publications

(30 citation statements)

References 20 publications

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“…Trisomy 7 has been reported in nonneoplastic renal proximal tubular cells [45], tumor-infiltrating lymphocytes [24], reactive noncancerous liver cells [6], smooth-muscle cells in atherosclerotic plaques [18], in placental cells in a case where the fetus had no chromosomal abnormality [74], in benign prostatic hyperplasia [2], and in many other noncancerous tissues [39]. Trisomy 7 has also very frequently been observed in premalignant cells and cancer cells of many types, including thyroid adenomas [7], colon adenomas [35], bladder cancer [56], breast cancer [15], prostate epithelial neoplasia (PIN) [61], prostate cancer [1,3,5,52,58,78], and many other cancers. Gain of chromosome 7 has also been observed in 30-56% of cases in three recent CGH studies in prostate cancer [19,40,71].…”

Section: Gain and Loss Of Chromosomementioning

confidence: 99%

Review of allelic loss and gain in prostate cancer

Bova

Isaacs²

1996

World J Urol

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There are three nearly ubiquitous genomic "imbalances" in prostate cancer cells: 1) loss of sequences from the short arm of chromosomes 8, 2) loss of sequences from the long arm of chromosome 13q, and 3) gain of sequences on the long arm of chromosome 8, particularly in advanced disease. Candidate tumor suppressor genes and oncogenes affected by this trio of consistent changes include the c-myc gene on chromosome 8q24, the RB gene at 13q14, and potentially multiple novel genes on the short arm of chromosome 8, with a gene located more proximally potentially involved in tumor initiation and a gene or genes located more distally involved in tumor progression. Loss of regions of chromosomes 2q, 5q, 6q, 7p and 7q, 9p, 10p and 10q, 16q, 17p and 17q, and 18q, and gain of regions of 1q, 2p, 3p and 3q, 7p and 7q, 11p, 17q, and Xq have also been detected in the range of 25-50% of tumors studied. Analysis of candidate tumor suppressor genes in these regions is still in its early stages. Similarly, potential oncogenes on a series of chromosomal arms which undergo frequent amplification remain essentially uncharacterized. The basic outline of the chromosomal aberrations in prostate cancer has been well established; the details of the story remain to be filled in. This paper reviews the advantages and disadvantages of various techniques for detection of genomic loss and gain in prostate cancer cells, and reviews published reports of loss and gain in prostate cancer, focusing primarily on reports using microsatellite analysis, Southern analysis, and comparative genomic hybridization. Fluorescence in situ hybridization (FISH) based analyses of selected regions are also reviewed.

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Section: Gain and Loss Of Chromosomementioning

confidence: 99%

Review of allelic loss and gain in prostate cancer

Bova

Isaacs²

1996

World J Urol

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“…After deparaffination with xylene (Merck, Darmstadt, Germany) and rehydration with ethanol (Merck) the tissue was incubated with proteinase K (200 pg/ml) (Sigma, St. Louis, MO, USA) (Korn et al, 1993). From the adenomas single cell suspensions (Herbergs et al, 1994) were prepared and these were subjected to proteinase K digestion.…”

Section: Dna Extractionmentioning

confidence: 99%

A detailed analysis of K-ras point mutations in relation to tumor progression and survival in colorectal cancer patients

et al. 1996

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“…The cutoff point for detection of a clone with ϩ7 was set at 10%, but the detected clones were in general large with a mean value of 57% of the cells counted (Table I). In a similar study using probes for chromosomes 1, 7, 17, X and Y, Herbergs et al 13 found ϩ7 in 13 of 35 (40%) colorectal adenomas. G-banding analyses have demonstrated that trisomy 7 is a very common finding in both adenomas and carcinomas of the large bowel 2, 14 -16 and that a subgroup of adenomas is characterized by having only numerical [34] changes, especially gain of chromosome 7.…”

Section: Discussionmentioning

confidence: 86%

“…The neoplasia-specificity of ϩ7 has been questioned, however, both in the context of colorectal carcinogenesis and in general. 27 Although both chromosome banding studies 28 and FISH analyses combined with immunocytochemistry 13,29 have demonstrated that the cells with ϩ7 belong to the epithelial component of colorectal adenomas, the pathogenetic role of this change in colorectal tumorigenesis remains unclear. Candidate genes have been identified in chromosome 7, 30 -33 but their actual role in tumorigenesis is unknown as is indeed the general mechanism by which gain of an extra whole chromosome turns the growth potential of a cell in the direction of neoplasia.…”

Section: Discussionmentioning

confidence: 99%

Assessments of clonal composition of colorectal adenomas by FISH analysis of chromosomes 1, 7, 13 and 20

et al. 2001

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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. Tumor progression is generally considered to be a multistep process characterized by the accumulation of genetic aberrations. 1 In the large bowel, early premalignant stages of tumorigenesis as well as later, malignant lesions are readily identified phenotypically as adenomas and adenocarcinomas. The acquired genetic aberrations characteristic of these 2 tumor types have been extensively examined at both the molecular genetic and cytogenetic level. The nonrandom changes thus revealed include, in carcinomas, structural rearrangements of chromosomes 1, 8, 13 and 17 and the numerical changes ϩ7, ϩ13, Ϫ17, Ϫ18, ϩ20, ϪY 1,2 and, in adenomas, gain of chromosomes 7, 13 and 20, loss of chromosome 18, as well as the structural rearrangements del(1p) and, less frequently, del(8p), i(13q), and del(17p). 2,3 Although no single cytogenetic aberration can be said to distinguish large bowel adenomas from carcinomas with absolute certainty, the former tumors generally have simpler karyotypes than do the malignant ones.The information value of the cytogenetic analysis of colorectal adenomas, as...

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Chromosome aberrations in adenomas of the colon. Proof of trisomy 7 in tumor cells by combined interphase cytogenetics and immunocytochemistry

Cited by 34 publications

References 20 publications

Review of allelic loss and gain in prostate cancer

Review of allelic loss and gain in prostate cancer

A detailed analysis of K-ras point mutations in relation to tumor progression and survival in colorectal cancer patients

Assessments of clonal composition of colorectal adenomas by FISH analysis of chromosomes 1, 7, 13 and 20

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