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  • 1.
    Adamovic, Tatjana
    et al.
    Med Coll Wisconsin, Human & Mol Genet Ctr, Milwaukee, WI 53226 USA.
    Hamta, Achmad
    Univ Gothenburg, CMB Genet, Gothenburg, Sweden.
    Roshani, Leyla
    Univ Gothenburg, CMB Genet, Gothenburg, Sweden.
    Lü, Xuschun
    Univ Gothenburg, CMB Genet, Gothenburg, Sweden.
    Röhme, Dan
    Univ Gothenburg, CMB Genet, Gothenburg, Sweden.
    Helou, Khalil
    Univ Gothenburg, Dept Oncol, Gothenburg, Sweden.
    Klinga-Levan, Karin
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Levan, Göran
    Univ Gothenburg, CMB Genet, Gothenburg, Sweden.
    Rearrangement and allelic imbalance on chromosome 5 leads to homozygous deletions in the CDKN2A/2B tumor suppressor gene region in rat endometrial cancer2008In: Cancer Genetics and Cytogenetics, ISSN 2210-7762, E-ISSN 2210-7770, Vol. 184, no 1, p. 9-21Article in journal (Refereed)
    Abstract [en]

    The inbred BDII rat is a valuable experimental model for the genetic analysis of hormone-dependent endometrial adenocarcinoma (EAC). One common aberration detected previously by comparative genomic hybridization in rat EAC is loss affecting mostly the middle part of rat chromosome 5 (RNO5). First, we applied an RNO5-specific painting probe and four region-specific gene probes onto tumor cell metaphases from 21 EACs, and found that rearrangements involving RNO5 were common. The copy numbers of loci situated on RNO5 were found to be reduced, particularly for the CDKN2A/2B locus. Second, polymerase chain reaction analysis was performed with 22 genes and markers and homozygous deletions of the CDKN2A exon 1β and CDKN2B genes were detected in 13 EACs (62%) and of CDKN2A exon 1α in 12 EACs (57%) Third, the occurrence of allelic imbalance in RNO5 was analyzed using 39 microsatellite markers covering the entire chromosome and frequent loss of heterozygosity was detected. Even more intriguing was the repeated finding of allele switching in a narrow region of 7 Mb across the CDKN2A/2B locus. We conclude that genetic events affecting the middle part of RNO5 (including bands 5q31q33 and the CDKN2A locus) contribute to the development of EAC in rat, with the CDKN2A locus having a primary role.

  • 2.
    Carlsson, Jessica
    et al.
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Helenius, Gisela
    Örebro University Hospital.
    Karlsson, Mats
    Örebro University Hospital.
    Lubovac, Zelmina
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Andrén, Ove
    Örebro University Hospital.
    Olsson, Björn
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Klinga-Levan, Karin
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Validation of suitable endogenous control genes for expression studies of miRNA in prostate cancer tissues2010In: Cancer Genetics and Cytogenetics, ISSN 2210-7762, E-ISSN 2210-7770, Vol. 202, no 2, p. 71-75Article in journal (Refereed)
    Abstract [en]

    When performing quantitative polymerase chain reaction analysis, there is a need for correction of technical variation between experiments. This correction is most commonly performed by using endogenous control genes, which are stably expressed across samples, as reference genes for normal expression in a specific tissue. In microRNA (miRNA) studies, two types of control genes are commonly used: small nuclear RNAs and small nucleolar RNAs. In this study, six different endogenous control genes for miRNA studies were investigated in prostate tissue material from the Swedish Watchful Waiting cohort. The stability of the controls was investigated using two different software applications, NormFinder and BestKeeper. RNU24 was the most suitable endogenous control gene for miRNA studies in prostate tissue materials.

  • 3.
    Karlsson, Elin
    et al.
    Department of Oncology, Institute of Clinical Sciences, Göteborg University, Blå stråket 2, SE-413 45 Göteborg, Sweden.
    Danielsson, Anna
    Department of Oncology, Institute of Clinical Sciences, Göteborg University, Blå stråket 2, SE-413 45 Göteborg, Sweden.
    Delle, Ulla
    Department of Oncology, Institute of Clinical Sciences, Göteborg University, Blå stråket 2, SE-413 45 Göteborg, Sweden.
    Olsson, Björn
    University of Skövde, School of Humanities and Informatics.
    Karlsson, Per
    Oncology Section, Department of Oncology, Sahlgrenska University Hospital, Blå stråket 2, SE-413 45 Göteborg, Sweden.
    Helou, Khalil
    Department of Oncology, Institute of Clinical Sciences, Göteborg University, Blå stråket 2, SE-413 45 Göteborg, Sweden.
    Chromosomal changes associated with clinical outcome in lymph node-negative breast cancer2007In: Cancer Genetics and Cytogenetics, ISSN 2210-7762, E-ISSN 2210-7770, Vol. 172, no 2, p. 139-146Article in journal (Refereed)
    Abstract [en]

    Breast cancer is the most common malignancy among women and accounts for over one million new cases worldwide per year. Lymph node-negative breast cancer patients are reputed as having a better prognosis than lymph node-positive ones. Around 20% of the lymph node-negative patients die within 10 years after diagnosis. To improve the prognostics of node-negative breast cancer, it is important to understand the underlying biologic mechanisms promoting survival, such as specific genetic changes in the tumor genome. In this study, CGH was applied to analyze 64 tumors from node-negative breast cancer patients to identify DNA copy number changes in chromosomes and chromosome regions that may be correlated to survival. The main findings show gains at 4q, 5q31not, vert, similarqter, 6q12not, vert, similarq16, and 12q14not, vert, similarq22, as well as losses of 17p, 18p, and Xq, which were significantly more recurrent in tumors from deceased patients than in tumors from survivors. The average number of chromosomal changes was higher in the tumors from deceased compared to the survivor tumors. Our findings suggest that tumors with specific chromosomal aberrations at 4q, 5q31not, vert, similarqter, 6q12not, vert, similarq16, 12q14not, vert, similarq22, 17p, 18p, and Xq result in an aggressive form of breast cancer and that these patients are predisposed to succumb to breast cancer.

  • 4.
    Karlsson, Sandra
    et al.
    University of Skövde, School of Life Sciences.
    Holmberg, Erik
    University of Skövde, School of Life Sciences.
    Askerlund, Anders
    University of Skövde, School of Life Sciences.
    Klinga-Levan, Karin
    University of Skövde, School of Life Sciences.
    Altered transforming growth factor-β pathway expression pattern in rat endometrial cancer2007In: Cancer Genetics and Cytogenetics, ISSN 2210-7762, E-ISSN 2210-7770, Vol. 177, no 1, p. 43-50Article in journal (Refereed)
    Abstract [en]

    Endometrial cancer is the most abundant female gynecologic malignancy, ranking fourth in incidence among invasive tumors in women. Females of the BDII inbred rat strain are extremely prone to endometrial adenocarcinoma (EAC), and approximately 90% of virgin females spontaneously develop EAC during their lifetime. Thus, these rats serve as a useful model for the genetic analysis of this malignancy. In the present work, gene expression profiling, by means of cDNA microarrays, was performed on cDNA from endometrial tumor cell lines and from cell lines derived from nonmalignant lesions/normal tissues of the endometrium. We identified several genes associated with the transforming growth factor-β (TGF-β) pathway to be differentially expressed between endometrial tumor cell lines and nonmalignant lesions by using clustering and statistical inference analyses. The expression levels of the genes involved in the TGF-β pathway were independently verified using semiquantitative reverse-transcription polymerase chain reaction. Repressed TGF-β signaling has been reported previously in EAC carcinogenesis, but this is the first report demonstrating aberrations in the expression of TGF-β downstream target genes. We propose that the irregularities present in TGF-β pathway among the majority of the EAC tumor cell lines may affect EAC carcinogenesis.

  • 5.
    Möllerström, Elin
    et al.
    University of Gothenburg.
    Delle, Ulla
    University of Gothenburg.
    Danielsson, Anna
    University of Gothenburg.
    Parris, Toshima
    University of Gothenburg.
    Olsson, Björn
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Karlsson, Per
    University of Gothenburg.
    Helou, Khalil
    University of Gothenburg.
    High-resolution genomic profiling to predict 10-year overall survival in node-negative breast cancer2010In: Cancer Genetics and Cytogenetics, ISSN 2210-7762, E-ISSN 2210-7770, Vol. 198, no 2, p. 79-89Article in journal (Refereed)
    Abstract [en]

    Women with clinically node-negative breast cancer have a better prognosis than do those with axillary lymph node metastasis. Nonetheless, ~20% of node-negative patients die within 15 years of diagnosis, and thus additional prognostic markers are greatly needed. To identify specific copy number alterations (CNAs) that differed in frequency between 10-year survivors and deceased patients with node-negative breast cancer, array comparative genomic hybridization (aCGH) was applied to 41 primary node-negative breast tumors. Fisher's exact test was used to identify significantly different CNAs between 10-year survivors and deceased patients. Losses at 8p21.2~p21.3, 8p23.1~p23.2, Xp21.3, and Xp22.31~p22.33 were significantly more common in tumors from deceased patients, suggesting that these alterations may contribute to tumor aggressiveness. Gains at 1q25.2~q25.3 and 1q31.3~q41 were more prevalent in tumors from survivors; specific gains at these genomic regions may inhibit further tumor progression, resulting in a less aggressive form of node-negative breast cancer. Evaluation of the identified CNAs in an independent external data set verified the prognistic potential of the 1q31.3~q41 region. Although further extensive validation is needed, the prognostic CNAs identified in this work may in time facilitate the clinical assessment of breast cancer.

  • 6.
    Nordlander, Carola
    et al.
    Lundberg Laboratory, CMB-Genetics, Göteborg Univ., Box 462, SE-40530 G., Sweden / Department of Pathology, Lundberg Lab. for Cancer Research, Göteborg, Sweden, Sweden.
    Behboudi, Afrouz
    Department of Pathology, Lundberg Lab. for Cancer Research, Göteborg, Sweden.
    Levan, Göran
    Lundberg Laboratory, CMB-Genetics, Göteborg Univ., Box 462, SE-40530 G., Sweden.
    Klinga Levan, Karin
    University of Skövde, School of Life Sciences.
    Allelic imbalance on chromosome 10 in rat endometrial adenocarcinomas2005In: Cancer Genetics and Cytogenetics, ISSN 2210-7762, E-ISSN 2210-7770, Vol. 156, no 2, p. 158-166Article in journal (Refereed)
    Abstract [en]

    Earlier work using comparative genome hybridization (CGH) has shown that rat chromosome 10 (RNO10) is frequently involved in cytogenetic aberrations in BDII rat endometrial adenocarcinomas (EAC). Relative reduction in copy number (chromosomal deletions) was seen in the proximal to middle part of the chromosome, whereas there were increases in copy number in the distal part. The occurrence of RNO10 aberrations was further analyzed in DNA from primary tumor material from 42 EACs and 3 benign endometrial tumors using allelotyping of microsatellite markers. We found frequently that there were 4 quite distinct RNO10 regions that exhibited allelic imbalance. Based on these findings we believe that genes with relevance to EAC tumor development are situated in each of these chromosome regions. Extrapolation of our microsatellite marker data to the rat draft DNA sequence will facilitate the definition of the regions at the level of the DNA and to select and characterize candidate genes within each of the affected chromosome regions.

  • 7.
    Roshani, L.
    et al.
    CMB-Genetics, Lundberg Laboratory, Göteborg University, Göteborg, Sweden.
    Mallon, P.
    Department of Animal Science, Medical School of Hannover, Hannover 30625, Germany.
    Sjöstrand, E.
    CMB-Genetics, Lundberg Laboratory, Göteborg University, Göteborg, Sweden.
    Wedekind, D.
    Department of Animal Science, Medical School of Hannover, Hannover 30625, Germany.
    Szpirer, J.
    Université Libre de Bruxelles, IBMM, Gosselies, Belgium.
    Szpirer, C.
    Université Libre de Bruxelles, IBMM, Gosselies, Belgium.
    Hedrich, H. J.
    University of Skövde, School of Life Sciences.
    Klinga-Levan, Karin
    University of Skövde, School of Life Sciences.
    Genetic analysis of susceptibility to endometrial adenocarcinoma in the BDII rat model2005In: Cancer Genetics and Cytogenetics, ISSN 2210-7762, E-ISSN 2210-7770, Vol. 158, no 2, p. 137-141Article in journal (Refereed)
    Abstract [en]

    Most cancers are genetically complex and heterogeneous, a serious obstacle to identifying specific genes underlying the disease. If inbred animal models are used, then both the genetic constitution and environmental influences can be carefully controlled. Females of the BDII inbred rat strain are genetically predisposed to endometrial cancer; more than 90% of virgin BDII females will develop endometrial adenocarcinoma (EAC) during their life span. BDII females were crossed to males from inbred strains with low EAC incidence (SPRD or BN). When F1 males were backcrossed to BDII females to generate N1 populations of offspring, about one fourth of the female progeny developed EAC. With transmission disequilibrium test analysis, significant association was detected in three chromosomal regions (on RNO1, RNO11, and RNO17) in the SPRD crosses and in the short arm of RNO20 in the BN crosses. It appears that several susceptibility genes with minor but cooperating effects are responsible for the susceptibility. Furthermore, it seems clear from the interstrain crosses not only that the onset of tumors depends on the presence of susceptibility alleles from the EAC-prone BDII strain, but also that tumor development is affected by the contribution of a genetic component derived from the nonsusceptible strains.

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