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Comparative genomic hybridization reveals a specific pattern of chromosomal gains and losses during the genesis of colorectal tumors
Author(s) -
Ried Thomas,
Knutzen Regina,
Steinbeck Rüdiger,
Blegen Harald,
Schröck Evelin,
Heselmeyer Kerstin,
du Manoir Stanislas,
Auer Gert
Publication year - 1996
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199604)15:4<234::aid-gcc5>3.0.co;2-2
Subject(s) - comparative genomic hybridization , biology , carcinogenesis , chromosome , aneuploidy , immunohistochemistry , ploidy , pathology , cancer research , microbiology and biotechnology , genetics , cancer , gene , medicine , immunology
Comparative genomic hybridization was used to screen the DNA extracted from histologically defined tissue sections from consecutive stages of colorectal carcinogenesis for chromosomal aberrations. No aberrations were detected in normal epithelium (n = 14). Gain of chromosome 7 occurred as a single event in low‐grade adenomas (n = 14). In high‐grade adenomas (n = 12), an overrepresentation of chromosomes 7 and 20 was present in 30% of the cases analyzed. The transition to colon carcinomas (n = 16) was characterized by the emergence of multiple chromosomal aberrations. Chromosomes 1, 13, and 20 and chromosome arms 7p and 8q were frequently gained, whereas chromosome 4 and chromosome arms 8p and 18q were recurrently underrepresented. The same tissue sections that were used for CGH were analyzed by means of DNA‐ploidy measurements and immunohistochemical staining to quantify proliferative activity and p21/WAF‐I and TP53 expression. We observed that crude aneuploidy and increased proliferative activity are early events in colorectal carcinogenesis, followed by TP53 overexpression and the acquisition of recurrent chromosomal gains and losses during the progression from high‐grade adenomas to invasive carcinomas. Genes Chromosom Cancer (1996). © 1996 Wiley‐Liss, Inc.