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.

Anti-leukemic activity of Dasatinib in both p53(wild-type) and p53 (mutated) B malignant cells.

BOSCO, Raffaella;VOLTAN, Rebecca;Celeghini C;CORALLINI, Federica;CAPITANI, Silvano;SECCHIERO, Paola
2012

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.
Bosco, Raffaella; Rabusin, M; Voltan, Rebecca; Celeghini, C; Corallini, Federica; Capitani, Silvano; Secchiero, Paola
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/1505324
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