| Literature DB >> 20953816 |
Raffaella Bosco1, Marco Rabusin, Rebecca Voltan, Claudio Celeghini, Federica Corallini, Silvano Capitani, Paola Secchiero.
Abstract
The multi-kinase inhibitor dasatinib induced a variable but significant decrease of viability in both p53(wild-type) (EHEB, JVM-2, JVM-3) and p53(mutated) (MEC-1, MEC-2, BJAB) prolymphocytic B leukemic cells, due to a combination of cell cycle block in G1 and apoptosis. Antibody phospho-kinase array analysis revealed that dasatinib inhibited the phosphorylation of various kinases, including ERK1/2 and p38/MAPK as well as of STAT3 transcription factors, in both p53(wild-type) and p53(mutated) cells. Therefore, dasatinib might offer a novel therapeutic strategy not only for p53(wild-type), but also for p53(mutated) B malignancies that have the worst prognosis and urgently need innovative therapeutic approaches.Entities:
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Year: 2010 PMID: 20953816 DOI: 10.1007/s10637-010-9564-6
Source DB: PubMed Journal: Invest New Drugs ISSN: 0167-6997 Impact factor: 3.850