Journal Article

DKFZ-2017-03015

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Arsenic trioxide inhibits tumor cell growth in malignant rhabdoid tumors in vitro and in vivo by targeting overexpressed Gli1.

Kerl, K. ; Moreno, N. ; Holsten, T. ; Ahlfeld, J. ; Mertins, J. ; Hotfilder, M. ; Kool, M.DKFZ* ; Bartelheim, K. ; Schleicher, S. ; Handgretinger, R. ; Schüller, U. ; Meisterernst, M. ; Frühwald, M. C.

2014
Wiley-Liss Bognor Regis

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Please use a persistent id in citations: doi:10.1002/ijc.28719

Abstract: Rhabdoid tumors are highly aggressive tumors occurring in infants and very young children. Despite multimodal and intensive therapy prognosis remains poor. Molecular analyses have uncovered several deregulated pathways, among them the CDK4/6-Rb-, the WNT- and the Sonic hedgehog (SHH) pathways. The SHH pathway is activated in rhabdoid tumors by GLI1 overexpression. Here, we demonstrate that arsenic trioxide (ATO) inhibits tumor cell growth of malignant rhabdoid tumors in vitro and in a mouse xenograft model by suppressing Gli1. Our data uncover ATO as a promising therapeutic approach to improve prognosis for rhabdoid tumor patients.

Keyword(s): Antineoplastic Agents ; Arsenicals ; GLI1 protein, human ; Gli protein, mouse ; Hedgehog Proteins ; Kruppel-Like Transcription Factors ; Oxides ; SHH protein, human ; Transcription Factors ; Zinc Finger Protein GLI1 ; arsenic trioxide

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Contributing Institute(s):

1. Pädiatrische Neuroonkologie (B062)

Research Program(s):

1. 312 - Functional and structural genomics (POF3-312) (POF3-312)

Appears in the scientific report 2014

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Database coverage:
; BIOSIS Previews ; Current Contents - Life Sciences ; IF >= 5 ; JCR ; NCBI Molecular Biology Database ; Nationallizenz ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection

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