PuSH - Publikationsserver des Helmholtz Zentrums München

Herold, T. ; Jurinovic, V.* ; Mulaw, M.A. ; Seiler, T. ; Dufour, A. ; Schneider, S. ; Kakadia, P.M. ; Feuring-Buske, M.* ; Braess, J. ; Spiekermann, K. ; Mansmann, U.* ; Hiddemann, W. ; Buske, C.* ; Bohlander, S.K.

Expression analysis of genes located in the minimally deleted regions of 13q14 and 11q22-23 in chronic lymphocytic leukemia - unexpected expression pattern of the RHO GTPase activator ARHGAP20.

Genes Chromosomes Cancer 50, 546-558 (2011)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
In chronic lymphocytic leukemia (CLL), 13q14 and 11q22-23 deletions are found in 2/3 of the cases. 11q22-23 deletions are associated with poor survival, whereas 13q14 deletions as single abnormality are often found in indolent disease forms. The molecular basis for this difference in prognosis is not known. We examined the 13q14 and 11q22-23 minimally deleted regions (MDRs) for differentially expressed genes by analyzing 154 microarray CLL gene expression data sets. We were able to generate a detailed gene expression map of the MDRs demonstrating a gene dosage effect. Surprisingly, ARHGAP20 encoding the RHO GTPase activating protein 20, which is located in the 11q22-23 MDR, showed-counterintuitively-a significantly higher expression in cases with 11q22-23 deletions compared with cases with no detectable genetic lesion or trisomy 12. Interestingly, cases with 13q14 deletions also had higher ARHGAP20 expression. These expression level changes were confirmed by quantitative PCR in 110 additional CLL samples. The ARHGAP20 gene encodes an evolutionarily conserved protein. In the zebra fish (Danio rerio) genome the syntenic regions of human chromosomal bands 13q14 and 11q22-23 are juxtaposed. The similar expression profiles of ARHGAP20 in 13q14 and 11q22-23 deleted CLL cases suggest a molecular connection and an intriguing mechanism of regulation.
Altmetric
Weitere Metriken?
[➜Einloggen]
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Genomic aberrations; Tumor-suppressor; Mutation status; Survival; Cancer; Identification; Micrornas; Diagnosis; Deletions; 11Q23
ISSN (print) / ISBN 1045-2257
e-ISSN 1098-2264
Zeitschrift Genes, Chromosomes and Cancer
Quellenangaben Band: 50, Heft: 7, Seiten: 546-558 Artikelnummer: , Supplement: ,
Verlag Wiley
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) CCG Pathogenesis of Acute Myeloid Leukemia (KKG-KPL)