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  • 1.
    Chen, Lei
    et al.
    University of Skövde, School of Humanities and Informatics.
    Nordlander, Carola
    CMB-Genetics, Lundberg Laboratory, Göteborg University, Göteborg, Sweden.
    Behboudi, Afrouz
    CMB-Genetics, Lundberg Laboratory, Göteborg University, Göteborg, Sweden.
    Olsson, Björn
    University of Skövde, School of Humanities and Informatics.
    Klinga Levan, Karin
    University of Skövde, School of Life Sciences.
    Deriving evolutionary tree models of the oncogenesis of endometrial adenocarcinoma2007In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 120, no 2, p. 292-296Article in journal (Refereed)
    Abstract [en]

    Endometrial adenocarcinoma (EAC) is the fourth leading cause of cancer death in women worldwide, but not much is known about the underlying genetic factors involved in the development of this complex disease. In the present work, we used 3 different algorithms to derive tree models of EAC oncogenesis from data on the frequencies of genomic alterations in rat chromosome 10 (RNO10). The tumor material was derived from progenies of crosses between the EAC susceptible BDII inbred rat strain and two non susceptible inbred rat strains. Data from allelic imbalance scans of RNO10 with microsatellite markers on solid tumor material and corresponding tissue cultures were used. For the analysis, RNO10 was divided into 24 segments containing a total of 59 informative microsatellite markers. The derived tree models show that genomic alterations have occurred in 11 of the 24 segments. In addition, the models provide information about the likely order of the alterations as well as their relationship with each other. Interestingly, there was a high degree of consistency among the different tree models and with the results of previous-studies, which supports the reliability of the tree models. Our results may be extended into a general approach for tree modeling of whole genome alterations during oncogenesis. (c) 2006 Wiley-Liss, Inc.

  • 2.
    Nordlander, Carola
    et al.
    CMB-Genetics, Lundberg Laboratory, Göteborg University, SE 40530 Gothenhurg, Sweden.
    Karlsson, Sandra
    University of Skövde, School of Life Sciences.
    Karlsson, Åsa
    CMB-Genetics, Lundberg Laboratory, Göteborg University, SE 40530 Gothenhurg, Sweden / Division of Medicine/Oncology, Stanford School of Medicine, Stanford, CA 94305, United States.
    Sjöling, Åsa
    Institute of Biomedicine, Department of Microbiology and Immunology, Göteborg University, SE 40530 Gothenburg, Sweden.
    Winnes, Marta
    CMB-Genetics, Lundberg Laboratory, Göteborg University, SE 40530 Gothenhurg, Sweden / Lundberg Laboratory for Cancer Research, Department of Pathology, Göteborg University, 41345 Gothenburg, Sweden.
    Klinga-Levan, Karin
    University of Skövde, School of Life Sciences.
    Behboudi, Afousz
    Institute of Biomedicine, Department of Clinical Genetics, Göteborg University, SE 40530 Gothenburg, Sweden / Institute of Biomedicine, Dept. Clinical Genetics, Göteborg University, 40530 Gothenburg, Sweden.
    Analysis of chromosome 10 aberrations in rat endometrial cancer: evidence for a tumor suppressor locus distal to Tp532007In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 120, no 7, p. 1472-1481Article in journal (Refereed)
    Abstract [en]

    We have recently shown in the BDII rat model of human endometrial adenocarcinoma (EAC), rat chromosome 10 (RNO10) is frequently involved in chromosomal aberrations. In the present study, we investigated the association between RNO10 deletions, allelic imbalance (AI) at RNO10q24 and Tp53 mutation in 27 rat EAC tumors. We detected chromosomal breakage accompanied by loss of proximal and/or gain of distal parts of RNO10 in approximately 2/3 of the tumors. This finding is suggestive of a tumor suppressor activity encoded from the proximal RNO10. Given the fact that Tp53 is located at RNO10q24-q25, we then performed Tp53 mutation analysis. However, we could not find a strong correlation between AI/deletions at RNO10q24 and Tp53 mutation. Instead, the observed patterns for AI, chromosomal breaks and deletions suggest that major selection was directed against a region located close to, but distal of Tp53. In different human malignancies a similar situation of AI at chromosome band 17p13.3 (HSA17p13.3) unassociated with TP53 mutation has been observed. Although RNO10 is largely homologous to HSA17, the conservation with respect to gene order among them is not extensive. We utilized publicly available draft DNA sequences to study intrachromosomal rearrangement during the divergence between HSA17 and RNO10. By using reciprocal comparison of rat and human genome data, we could substantially narrow down the candidate tumor suppressor region in rat from 3 Mb to a chromosomal segment of about 0.5 Mb in size. These results provide scientific groundwork for identification of the putative tumor suppressor gene(s) at 17p13.3 in human tumors

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