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

The STAT5 inhibitor pimozide decreases survival of chronic myelogenous leukemia cells resistant to kinase inhibitors

14 Jan 2011

Abstract excerpt

The transcription factor STAT5 is an essential mediator of the pathogenesis of chronic myelogenous leukemia (CML). In CML, the BCR/ABL fusion kinase causes the constitutive activation of STAT5, thereby driving the expression of genes promoting survival. BCR/ABL kinase inhibitors have become the mainstay of therapy for CML, although CML cells can develop resistance through mutations in BCR/ABL. To overcome this...

Read the complete abstract on PubMed

Topics

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

Share to Chronic Lymphocytic Leukemia Research
Share to Chronic Myeloid Leukemia Treatments
Share to Eosinophilic Disorders and Syndromes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 21233313
DOI: 10.1182/blood-2009-11-255232

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The STAT5 inhibitor pimozide decreases survival of chronic myelogenous leukemia cells resistant to kinase inhibitorsPMID 21233313Read ↗

The Antineoplastic Role of STAT5 Inhibition in BCRABL1-Positive Cells Exposed to Pimozide Alone and in Combination with Dasatinib and PonatinibSemantic proximity Read ↗

The PIM kinases in hematological cancersSemantic proximity Read ↗

Targeting PIM kinases impairs survival of hematopoietic cells transformed by kinase inhibitor-sensitive and kinase inhibitor-resistant forms of Fms-like tyrosine kinase 3 and BCR/ABL.Semantic proximity Read ↗

Targeting PIM Kinases to Overcome Therapeutic Resistance in CancerSemantic proximity Read ↗

Pre-clinical evidence of PIM kinase inhibitor activity in BCR-ABL1 unmutated and mutated Philadelphia chromosome-positive (Ph+) leukemias.Semantic proximity Read ↗

Direct STAT3 and STAT5 Inhibition Overcomes Treatment Resistance in a Murine-Derived in vitro Model of Acute Lymphoblastic Leukaemia Driven by <italic>ETV6::JAK2</italic>.Semantic proximity Read ↗

IRF5 is a target of BCR-ABL kinase activity and reduces CML cell proliferationSemantic proximity Read ↗

Fighting Tumor Cell Survival: Advances in the Design and Evaluation of Pim InhibitorsSemantic proximity Read ↗

A potential therapeutic target for FLT3-ITD AML: PIM1 kinase.Semantic proximity Read ↗

Sensitivity of imatinib-resistant T315I BCR-ABL CML to a synergistic combination of ponatinib and forskolin treatment.Semantic proximity Read ↗

CaMKII γ, a critical regulator of CML stem/progenitor cells, is a target of the natural product berbamine.Semantic proximity Read ↗

A Chemical Biology Approach to Developing STAT Inhibitors: Molecular Strategies for Accelerating Clinical TranslationSemantic proximity Read ↗

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