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Overrepresentation of 3q and 8q material and loss of 18q material are recurrent findings in advanced human ovarian cancer
Author(s) -
Arnold Norbert,
Hägele Lorenz,
Walz Lioba,
Schempp Werner,
Pfisterer Jacobus,
Bauknecht Thomas,
Kiechle Marion
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(199605)16:1<46::aid-gcc7>3.0.co;2-3
Subject(s) - comparative genomic hybridization , carcinogenesis , biology , chromosome , ovarian cancer , cancer , cancer research , genetics , gene , ovarian tumor , cytogenetics , microbiology and biotechnology
In order to define the ability of comparative genomic hybridization (CGH) to detect and map genetic imbalances, we investigated 47 malignant ovarian tumors and 2 ovarian tumors of low malignant potential. The most common genetic changes in order of frequency included DNA gains of chromosome arms 8q (53%), 3q (51%), 20q (43%), 1p (32%), 19q (30%), 1q (28%), 12p (28%), 6p (21%), and 2q (19%). The smallest regions of overrepresentation could be defined in 3q26‐qter, 8q23‐qter, 1p35‐pter, 12p12, and 6p21‐22, respectively. Losses were detected on 18q (23%), chromosome 4 (23%), 13q (17%), and 16q (17%) with the smallest underrepresented regions on 18q22‐qter, 13q21, and 16q23‐qter. Also, losses of the X chromosome (19%) were detected, correlating with higher ages of the patients. Therefore, some of these X chromosome losses might be due to a well‐known aging phenomenon and in these cases will be more preferably lost during cell division and tumor progression. Our findings show that ovarian carcinomas reveal consistent chromosomal abnormalities. Further detailed studies of these regions with specific molecular genetic techniques may lead to the identification of oncogenes and/or tumor suppressor genes playing an important role in the tumorigenesis of ovarian carcinomas. Genes Chromosom Cancer 16:46–54 (1996) . © 1996 Wiley‐Liss, Inc.