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10.1158/0008-5472.CAN-05-4528 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-05-4528 16778176!ä!16778176 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=16778176&cmd=llinks): Failed to open stream: HTTP request failed! 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Multiple imprinted and stemness genes provide a link between normal and tumor progenitor cells of the developing human kidney |pdf=|usr=}}{{16778176}} gab.com Text Multiple imprinted and stemness genes provide a link between normal and tumor progenitor cells of the developing human kidney JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=16778176 #FOAvip Wilms' tumor (WT), the embryonic kidney malignancy, is suggested to evolve from a progenitor cell population of uninduced metanephric blastema, which typically gives rise to nephrons. However, apart from blastema, WT specimens frequently contain cells that have differentiated into renal tubular or stromal phenotypes, complicating their analysis. We aimed to define tumor-progenitor genes that function in normal kidney development using WT xenografts (WISH-WT), in which the blastema accumulates with serial passages at the expense of differentiated cells. Herein, we did transcriptional profiling using oligonucleotide microarrays of WISH-WT, WT source, human fetal and adult kidneys, and primary and metastatic renal cell carcinoma. Among the most significantly up-regulated genes in WISH-WT, we identified a surprising number of paternally expressed genes (PEG1/MEST, PEG3, PEG5/NNAT, PEG10, IGF2, and DLK1), as well as Meis homeobox genes [myeloid ecotropic viral integration site 1 homologue 1 (MEIS1) and MEIS2], which suppress cell differentiation and maintain self-renewal. A comparison between independent WISH-WT and WT samples by real-time PCR showed most of these genes to be highly overexpressed in the xenografts. Concomitantly, they were significantly induced in human fetal kidneys, strictly developmentally regulated throughout mouse nephrogenesis and overexpressed in the normal rat metanephric blastema. Furthermore, in vitro differentiation of the uninduced blastema leads to rapid down-regulation of PEG3, DLK1, and MEIS1. Interestingly, ischemic/reperfusion injury to adult mouse kidneys reinduced the expression of PEG3, PEG10, DLK1, and MEIS1, hence simulating embryogenesis. Thus, multiple imprinted and stemness genes that function to expand the renal progenitor cell population may lead to evolution and maintenance of WT. Twit Text FOAVip Multiple imprinted and stemness genes provide a link between normal and tumor progenitor cells of the developing human kidney ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=16778176 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=16778176 #FOAvip English Wikipedia <ref>{{Cite pmid|16778176}}</ref> Multiple imprinted and stemness genes provide a link between normal and tumor progenitor cells of the developing human kidney #MMPMID16778176 Dekel B; Metsuyanim S; Schmidt-Ott KM; Fridman E; Jacob-Hirsch J; Simon A; Pinthus J; Mor Y; Barasch J; Amariglio N; Reisner Y; Kaminski N; Rechavi G Cancer Res 2006[Jun]; 66 (12): 6040-9 PMID16778176show ga Wilms' tumor (WT), the embryonic kidney malignancy, is suggested to evolve from a progenitor cell population of uninduced metanephric blastema, which typically gives rise to nephrons. However, apart from blastema, WT specimens frequently contain cells that have differentiated into renal tubular or stromal phenotypes, complicating their analysis. We aimed to define tumor-progenitor genes that function in normal kidney development using WT xenografts (WISH-WT), in which the blastema accumulates with serial passages at the expense of differentiated cells. Herein, we did transcriptional profiling using oligonucleotide microarrays of WISH-WT, WT source, human fetal and adult kidneys, and primary and metastatic renal cell carcinoma. Among the most significantly up-regulated genes in WISH-WT, we identified a surprising number of paternally expressed genes (PEG1/MEST, PEG3, PEG5/NNAT, PEG10, IGF2, and DLK1), as well as Meis homeobox genes [myeloid ecotropic viral integration site 1 homologue 1 (MEIS1) and MEIS2], which suppress cell differentiation and maintain self-renewal. A comparison between independent WISH-WT and WT samples by real-time PCR showed most of these genes to be highly overexpressed in the xenografts. Concomitantly, they were significantly induced in human fetal kidneys, strictly developmentally regulated throughout mouse nephrogenesis and overexpressed in the normal rat metanephric blastema. Furthermore, in vitro differentiation of the uninduced blastema leads to rapid down-regulation of PEG3, DLK1, and MEIS1. Interestingly, ischemic/reperfusion injury to adult mouse kidneys reinduced the expression of PEG3, PEG10, DLK1, and MEIS1, hence simulating embryogenesis. Thus, multiple imprinted and stemness genes that function to expand the renal progenitor cell population may lead to evolution and maintenance of WT. |*Genomic Imprinting[MESH] |Animals[MESH] |Gene Expression Profiling[MESH] |Homeodomain Proteins/biosynthesis/genetics[MESH] |Humans[MESH] |Kidney Neoplasms/*genetics[MESH] |Kidney/embryology/growth & development[MESH] |Mice[MESH] |Mice, Inbred BALB C[MESH] |Mice, Nude[MESH] |Mice, SCID[MESH] |Multigene Family[MESH] |Myeloid Ecotropic Viral Integration Site 1 Protein[MESH] |Neoplasm Proteins/biosynthesis/genetics[MESH] |Neoplasm Transplantation[MESH] |Neoplastic Stem Cells[MESH] |Oligonucleotide Array Sequence Analysis[MESH] |Rats[MESH] |Transplantation, Heterologous[MESH]Multiple imprinted and stemness genes provide a link between normal an(epmc).pdf DeepDyve Pubget Overpricing