<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">VLADUŠIĆ, TOMISLAV</style></author><author><style face="normal" font="default" size="100%">HRAŠĆAN, RENO</style></author><author><style face="normal" font="default" size="100%">KRUŠLIN, BOŽO</style></author><author><style face="normal" font="default" size="100%">PEĆINA-ŠLAUS, NIVES</style></author><author><style face="normal" font="default" size="100%">PERICA, KRISTINA</style></author><author><style face="normal" font="default" size="100%">BIĆANIĆ, ANAMARIJA</style></author><author><style face="normal" font="default" size="100%">VRHOVAC, IVANA</style></author><author><style face="normal" font="default" size="100%">GAMULIN, MARIJA</style></author><author><style face="normal" font="default" size="100%">FRANEKIĆ, JASNA</style></author></authors><secondary-authors></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Histological Groups of Human Postpubertal Testicular Germ Cell Tumours Harbour Different Genetic Alterations</style></title><secondary-title><style face="normal" font="default" size="100%">Anticancer Research</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014-08-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">4005-4012</style></pages><volume><style face="normal" font="default" size="100%">34</style></volume><issue><style face="normal" font="default" size="100%">8</style></issue><abstract><style  face="normal" font="default" size="100%">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.</style></abstract></record></records></xml>