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Cytogenetic aberrations in spontaneous endometrial adenocarcinomas in the BDII rat model as revealed by chromosome banding and comparative genome hybridization
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- Hamta, Ahmad, 1961 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för cell- och molekylärbiologi,Institutionen för laboratoriemedicin , Avdelningen för patologi,Department of Cell and Molecular Biology,Institute of Laboratory Medicine, Dept of Pathology
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- Adamovic, Tatjana, 1974 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för laboratoriemedicin , Avdelningen för patologi,Institutionen för cell- och molekylärbiologi,Institute of Laboratory Medicine, Dept of Pathology,Department of Cell and Molecular Biology
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- Helou, Khalil, 1966 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för särskilda specialiteter, Avdelningen för onkologi,Institute of Selected Clinical Sciences, Department of Oncology
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- 2005
- 2005
- English.
- In: Cancer Genet Cytogenet. ; 159:2, s. 123-8
- Journal article (peer-reviewed)
Abstract
Subject headings
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- Female rats of the inbred strain BDII are genetically predisposed to endometrial estrogen-dependent adenocarcinomas (EAC). More than 90% of them spontaneously develop this tumor type before the age of 24 months. In order to dissect out the genetic components behind these tumors we have made crosses between BDII females and rats from 2 other strains that are nonsusceptible to EAC. It was found that EAC tumors developed in a subset of intercross and backcross animals from both interstrain crosses. The chromosomal changes in the developing tumors were studied using cytogenetic and molecular cytogenetic methods. From these studies, we conclude that certain chromosome regions were recurrently engaged in chromosomal changes such as increases in copy number (e.g., trisomy, amplification) or decreases (e.g., deletion). Based on the analysis of 56 tumors, 8 regions were found to be particularly often involved: RNO4prx, gain=34 (61%) (amplification 12 cases); RNO5mid, loss=15 (27%); RNO6prx, gain=25 (45%) (amplification 8 cases); RNO10 loss, prx-mid/gain dst=25 (45%) (amplification 1 case); RNO12q, gain=23 (41%); RNO15p loss/RNO15q gain=29 (52%) (amplification 1 case) [RNO, rat chromosome; prx, proximal; mid, middle; dst, distal; p, short arm; q, long arm]. We begun to analyze these regions in detail using various molecular methods and within them there are certain possible target genes, such as MET (RNO4q21), CDKN2A/2B (RNO5q32), MYCN (RNO6q15 approximately q16), and TP53 (RNO10q24 approximately q25), but it is clear that several other genes, still unidentified, must also be involved.
Subject headings
- NATURVETENSKAP -- Biologi -- Genetik (hsv//swe)
- NATURAL SCIENCES -- Biological Sciences -- Genetics (hsv//eng)
Keyword
- Adenocarcinoma/*genetics
- Animals
- *Chromosome Aberrations
- Chromosome Banding
- Crosses
- Genetic
- Endometrial Neoplasms/*genetics
- Female
- Gene Dosage
- Male
- Nucleic Acid Hybridization/methods
- Rats
- Rats
- Inbred Strains
Publication and Content Type
- ref (subject category)
- art (subject category)
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