Tomislav Vladušić1, Reno Hrašćan2, Božo Krušlin3, Nives Pećina-Šlaus4, Kristina Perica2, Anamarija Bićanić2, Ivana Vrhovac5, Marija Gamulin6, Jasna Franekić2. 1. Department of Biochemical Engineering, Faculty of Food Technology and Biotechnology, University of Zagreb, Zagreb, Croatia tvladusic@pbf.hr. 2. Department of Biochemical Engineering, Faculty of Food Technology and Biotechnology, University of Zagreb, Zagreb, Croatia. 3. Ljudevit Jurak Department of Pathology, Sisters of Mercy University Hospital, Zagreb, Croatia School of Medicine, University of Zagreb, Zagreb, Croatia. 4. Laboratory of Neurooncology, Croatian Institute for Brain Research, Zagreb, Croatia School of Medicine, University of Zagreb, Zagreb, Croatia. 5. Institute for Medical Research and Occupational Health, Zagreb, Croatia. 6. Department of Oncology, Rebro University Hospital Center, Zagreb, Croatia.
Abstract
BACKGROUND: Testicular germ cell tumours are the most common malignancies in young males. Molecular biology studies of these tumours are often contradictory. Two histological groups, seminoma and non-seminoma, differ both morphologically and in malignant behaviour. Although a common cytogenetic feature is seen, namely the amplification of the 12p chromosomal region, the development mechanisms of less aggressive seminomas and more aggressive non-seminomas are unknown. MATERIALS AND METHODS: Occurrence of structural genetic alterations was analyzed in 18 seminomas and 22 non-seminomas for genes involved in the malignant tumour phenotype: cadherin 1, Type 1, E-cadherin (Epithelial), CDH1; adenomatous polyposis coli, APC; NME/NM23 nucleoside diphosphate kinase 1, NME1; tumour protein P53, TP53; cyclin-dependent kinase inhibitor 2A, CDKN2A; retinoblastoma 1, RB1; RAD51 recombinase, RAD51; mutS homolog 2, MSH2; MutL homolog 1, MLH1; breast cancer 1, early onset, BRCA1; BCL2-Associated X Protein, BAX; ATP-Binding Cassette, Sub-Family G (WHITE), Member 2, ABCG2. Genetic alterations, loss of heterozygosity and microsatellite instability, were analyzed using restriction fragment or microsatellite repeat length polymorphisms. RESULTS: A difference in genetic alteration occurrence between seminomas and non-seminomas was observed. CONCLUSION: Occurrence of genetic alterations correlates with clinical behaviour of these tumours and may indicate that such alterations could occur early in the development of seminomas and non-seminomas. Copyright
BACKGROUND:Testicular germ cell tumours are the most common malignancies in young males. Molecular biology studies of these tumours are often contradictory. Two histological groups, seminoma and non-seminoma, differ both morphologically and in malignant behaviour. Although a common cytogenetic feature is seen, namely the amplification of the 12p chromosomal region, the development mechanisms of less aggressive seminomas and more aggressive non-seminomas are unknown. MATERIALS AND METHODS: Occurrence of structural genetic alterations was analyzed in 18 seminomas and 22 non-seminomas for genes involved in the malignant tumour phenotype: cadherin 1, Type 1, E-cadherin (Epithelial), CDH1; adenomatous polyposis coli, APC; NME/NM23 nucleoside diphosphate kinase 1, NME1; tumour protein P53, TP53; cyclin-dependent kinase inhibitor 2A, CDKN2A; retinoblastoma 1, RB1; RAD51 recombinase, RAD51; mutS homolog 2, MSH2; MutL homolog 1, MLH1; breast cancer 1, early onset, BRCA1; BCL2-Associated X Protein, BAX; ATP-Binding Cassette, Sub-Family G (WHITE), Member 2, ABCG2. Genetic alterations, loss of heterozygosity and microsatellite instability, were analyzed using restriction fragment or microsatellite repeat length polymorphisms. RESULTS: A difference in genetic alteration occurrence between seminomas and non-seminomas was observed. CONCLUSION: Occurrence of genetic alterations correlates with clinical behaviour of these tumours and may indicate that such alterations could occur early in the development of seminomas and non-seminomas. Copyright
Authors: Dora Markulin; Aleksandar Vojta; Ivana Samaržija; Marija Gamulin; Ivona Bečeheli; Irena Jukić; Čedomir Maglov; Vlatka Zoldoš; Aleksandra Fučić Journal: Cancer Genomics Proteomics Date: 2017 Sep-Oct Impact factor: 4.069