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  • 1.
    Adamovic, Tatjana
    et al.
    University of Skövde, School of Technology and Society.
    Roshani, Leyla
    CMB-Genetics, Göteborg University, SE 40530 Göteborg, Sweden / Department of Clinical Genetics, Göteborg University, SE 40530 Göteborg, Sweden.
    Chen, Lei
    University of Skövde, School of Humanities and Informatics.
    Schaffer, Beverly S.
    Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE 68198, United States / Eppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, NE 68198, United States.
    Helou, Khalil
    Department of Oncology, Göteborg University, Sahlgrenska University, Göteborg, Sweden.
    Levan, Göran
    CMB-Genetics, Göteborg University, SE 40530 Göteborg, Sweden / Department of Clinical Genetics, Göteborg University, SE 40530 Göteborg, Sweden.
    Olsson, Björn
    University of Skövde, School of Humanities and Informatics.
    Schull, James D.
    Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE 68198, United States / Eppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, NE 68198, United States / Department of Genetics, Cell Biology and Anatomy, 6005 Durham Research Center, 985805 Nebraska Medical Center, Omaha, NE 68198-5805, United States.
    Nonrandom pattern of aberrations in 17β-estradiol-induced rat mammary tumors: Indications of distinct pathways for tumor development2007In: Genes, Chromosomes and Cancer, ISSN 1045-2257, E-ISSN 1098-2264, Vol. 46, no 5, p. 459-469Article in journal (Refereed)
    Abstract [en]

    Estrogens play an important role in breast cancer etiology and the ACI rat provides a novel animal model for defining the mechanisms through which estrogens contribute to mammary cancer development. In crossing experiments between the susceptible ACI strain and two resistant strains, COP (Copenhagen) and BN (Brown Norway), several quantitative trait loci (QTL) that affect development of 17b-estradiol (E2)-induced mammary tumors have been defined. Using comparative genomic hybridization (CGH), we have analyzed cytogenetic aberrations in E2-induced mammary cancers and have found clear patterns of nonrandom chromosomal involvement. Approximately two thirds of the tumors exhibited copy number changes. Losses of rat chromosome 5 (RNO5) and RNO20 were particularly common, and it was found that these two aberrations often occurred together. A third recurrent aberration involving proximal gain and distal loss in RNO6 probably defined a distinct subgroup of tumors, since it never occurred in combination with RNO5 loss. Interestingly, QTL with powerful effects on mammary cancer development have been mapped to RNO5 and RNO6. These findings suggest that there were at least two genetic pathways to tumor formation in this rat model of E2-induced mammary cancer. By performing CGH on mammary tumors from ACI rats, F1 rats from crosses between the ACI and COP or BN strains and ACI.BN-Emca8 congenic rats, which carry the BN allele of the Emca8 QTL on RNO5 on the ACI genetic background, we were able to determine that the constitution of the germ line influences the pattern of chromosomal aberrations.

  • 2.
    Adamovic, Tatjana
    et al.
    Department of Pathology, Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden / CMB-Genetics, Department of Pathology, Göteborg University, SE 41345 Göteborg, Sweden.
    Trossö, Fredrik
    University of Skövde, School of Life Sciences.
    Roshani, Leyla
    Department of Pathology, Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden.
    Andersson, Lars
    CMB-Genetics, Lundberg Laboratory, Göteborg University, Göteborg, Sweden.
    Petersen, Greta
    CMB-Genetics, Lundberg Laboratory, Göteborg University, Göteborg, Sweden.
    Rajaei, Saide
    Department of Pathology, Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden.
    Helou, Khalil
    Department of Oncology, Göteborg University, Sahlgrenska University, Göteborg, Sweden.
    Levan, Göran
    Department of Pathology, Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden.
    Oncogene amplification in the proximal part of chromosome 6 in rat endometrial adenocarcinoma as revealed by combined BAC/PAC FISH, chromosome painting, zoo-FISH, and allelotyping2005In: Genes, Chromosomes and Cancer, ISSN 1045-2257, E-ISSN 1098-2264, Vol. 44, no 2, p. 139-153Article in journal (Refereed)
    Abstract [en]

    The inbred BDII rat is a valuable experimental model for the genetic analysis of endometrial adenocarcinoma (EAC). One common aberration detected by comparative genomic hybridization in rat EAC was gain/amplification affecting the proximal part of rat chromosome 6 (RNO6). We applied rat and mouse chromosome painting probes onto tumor cell metaphase preparations in order to detect and characterize gross RNO6 aberrations. In addition, the RNO6q11-q16 segment was analyzed by fluorescence in situ hybridization with probes representing 12 cancer-related genes in the region. The analysis revealed that seven tumors contained large RNO6-derived homogeneously staining regions (HSRs) in addition to several normal or near-normal RNO6 chromosomes. Five tumors (two of which also had HSRs) exhibited a selective increase of the RNO6q11-q16 segment, sometimes in conjunction with moderate amplification of one or a few genes. Most commonly, the amplification affected the region centered around band 6q16 and included the Mycn, Ddx1, and Rrm2 genes. A second region, centering around Slc8a1 and Xdh, also was affected by gene amplification but to a lesser extent. The aberrations in the proximal part of RNO6 were further analyzed using allelotyping of microsatellite markers in all tumors from animals that were heterozygous in the proximal RNO6 region. We could detect allelic imbalance (AI) in 12 of 20 informative tumors, 6 of which were in addition to those already analyzed by molecular cytogenetic methods as described. Our findings suggest that increase/amplification of genes in this chromosome region contribute to the development of this hormone-dependent tumor.

  • 3.
    Falck, Eva
    et al.
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Behboudi, Afrouz
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Klinga-Levan, Karin
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    The impact of the genetic background on the genome make-up of tumor cells2012In: Genes, Chromosomes and Cancer, ISSN 1045-2257, E-ISSN 1098-2264, Vol. 51, no 5, p. 438-446Article in journal (Refereed)
    Abstract [en]

    Endometrial adenocarcinoma (EAC) is the most common form of malignancy in the female genital tract, ranking as the fourth leading form of invasive tumors that affect women. The BDII inbred rat strain has been used as a powerful tumor model in studies of the genetic background of EAC. Females from the BDII strain are prone to develop tumors with an incidence of more than 90%. Development of EAC in BDII female rats has similarities in pathogenesis, histopathological, and molecular properties to that of human, and thus represents a unique model for analysis of EAC tumorigenesis and for comparative studies in human EACs. In a previous study, a set of rat EAC cell lines derived from tumors developed in female crossprogenies between BDII and nonsusceptible rat strains were analyzed by spectral karyotyping (SKY). Here we present an analysis with specific focus on the impact of different genetic backgrounds on the rate and occurrence of genetic aberrations in experimental tumors using data presented in the previous report. We could reveal that the ploidy state, and the abundance and type of structural as well as numerical change differed between the two genetic setups. We have also identified chromosomes harboring aberrations independent of genetic input from the nonsusceptible strains, which provide valuable information for the identification of the genes involved in the development of EAC in the BDII model as well as in human endometrial tumors. (C) 2012 Wiley Periodicals, Inc.

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