Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

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

Investigational new drugs - 1 Feb 2012

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

Abstract excerpt

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...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Dasatinib
Share to G1 Phase Cell Cycle Checkpoints

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mitogen-Activated Protein Kinase 1

Share to Mitogen-Activated Protein Kinase 3

Share to p38 Mitogen-Activated Protein Kinases

Share to Pyrimidines

Share to STAT3 Transcription Factor

Share to Thiazoles

Source

Identifiers

PMID: 20953816
DOI: 10.1007/s10637-010-9564-6

Genes

STAT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Anti-leukemic activity of dasatinib in both p53(wild-type) and p53(mutated) B malignant cells.PMID 20953816Read ↗

Dasatinib plus Nutlin-3 shows synergistic antileukemic activity in both p53 wild-type and p53 mutated B chronic lymphocytic leukemias by inhibiting the Akt pathway.Semantic proximity Read ↗

The kinase inhibitor dasatinib induces apoptosis in chronic lymphocytic leukemia cells in vitro with preference for a subgroup of patients with unmutated IgVH genesSemantic proximity Read ↗

Molecular characterization and therapeutic reaction to dasatinib in a CML patient harboring a novel e8a2 BCR-ABL1 transcript with a somatic mutation in TP53BP2 and cadherin-10 genes.Semantic proximity Read ↗

Dasatinib treatment for Philadelphia chromosome‐positive leukemiasSemantic proximity Read ↗

Abcg2 overexpression represents a novel mechanism for acquired resistance to the multi-kinase inhibitor Danusertib in BCR-ABL-positive cells in vitro.Semantic proximity Read ↗

The development of dasatinib as a treatment for chronic myeloid leukemia (CML): from initial studies to application in newly diagnosed patients.Semantic proximity Read ↗

TP53-agnostic lethality through combined pan-HDAC and CDK inhibition in acute myeloid leukemia.Semantic proximity Read ↗

Hitting two oncogenic machineries in cancer cells: cooperative effects of the multi-kinase inhibitor ponatinib and the BET bromodomain blockers JQ1 or dBET1 on human carcinoma cellsSemantic proximity Read ↗

Targeting the p53-MDM2 interaction by the small-molecule MDM2 antagonist Nutlin-3a: a new challenged target therapy in adult Philadelphia positive acute lymphoblastic leukemia patientsSemantic proximity Read ↗

AZD5153: A Novel Bivalent BET Bromodomain Inhibitor Highly Active against Hematologic MalignanciesSemantic proximity Read ↗

All tyrosine kinase inhibitor-resistant chronic myelogenous cells are highly sensitive to ponatinib.Semantic proximity Read ↗

The oncogene DEK promotes leukemic cell survival and is downregulated by both Nutlin-3 and chlorambucil in B-chronic lymphocytic leukemic cells.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.