title: Recurrent gene amplifications in human type I endometrial adenocarcinoma detected by fluorescence in situ hybridization.
abstract: Determining what genes are actively involved in tumor development is important, because they may provide targets for directed therapy. Human tumors are greatly heterogeneous with respect to etiology and genetic background, which complicates the identification of common genetic aberrations. In contrast, genetic and environmental variation can be in part controlled in experimental animals, which facilitates identification of the important changes. In inbred BDII rats, which are genetically predisposed to endometrial adenocarcinomas (EAC), certain chromosome regions exhibit recurrent amplification in the tumors. Previous CGH analysis had shown that a subset of human EAC tumors exhibited increased copy numbers in the homologous chromosomal regions, located in human 2p21 approximately p25 and 7q21 approximately q31. Using fluorescence in situ hybridization analysis on imprints from 13 human EAC tumors, we determined the average copy numbers of each of 15 probes derived from cancer-related genes situated in these chromosome regions. Among the genes analyzed, those most often targeted by amplification were SDC1 and CYP1B1 in 2p21 approximately p25 and CDK6 and MET in 7q21 approximately q31, but all of the 15 genes tested were found to be amplified in at least two tumors.
authors.affiliation: CMB-Genetics, Lundberg Laboratory, Göteborg University, Box 462, SE-405 30 Göteborg, Sweden. Emma.Samuelson@gu.se
authors.forename: Emma
authors.initials: E
authors.lastname: Samuelson
authors.forename: Kristina
authors.initials: K
authors.lastname: Levan
authors.forename: Tatjana
authors.initials: T
authors.lastname: Adamovic
authors.forename: Göran
authors.initials: G
authors.lastname: Levan
authors.forename: György
authors.initials: G
authors.lastname: Horvath
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics* / Q000473:pathology; D001189:Aryl Hydrocarbon Hydroxylases / Q000235:genetics; D002874:Chromosome Mapping; D003001:Cloning, Molecular; D051361:Cyclin-Dependent Kinase 6 / Q000235:genetics; D065633:Cytochrome P-450 CYP1B1; D016889:Endometrial Neoplasms / Q000235:genetics* / Q000473:pathology; D005260:Female; D005784:Gene Amplification; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D009367:Neoplasm Staging; D009693:Nucleic Acid Hybridization; D011518:Proto-Oncogene Proteins / Q000235:genetics; D019859:Proto-Oncogene Proteins c-met; D017978:Receptors, Growth Factor / Q000235:genetics; D053668:Syndecan-1 / Q000235:genetics
chemical_list: D011518:Proto-Oncogene Proteins; D017978:Receptors, Growth Factor; C508241:SDC1 protein, human; D053668:Syndecan-1; D001189:Aryl Hydrocarbon Hydroxylases; C585496:CYP1B1 protein, human; C585499:Cyp1b1 protein, rat; D065633:Cytochrome P-450 CYP1B1; C491743:MET protein, human; D019859:Proto-Oncogene Proteins c-met; D051361:Cyclin-Dependent Kinase 6