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

Raffaella Bosco, Marco Rabusin, Rebecca Voltan, Claudio Celeghini, Federica Corallini, Silvano Capitani, Paola Secchiero

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)417-422
Number of pages6
JournalInvestigational New Drugs
Issue number1
Publication statusPublished - Feb 2012


  • Dasatinib
  • Leukemic cells
  • p53

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)
  • Oncology


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