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

Disrupting BCR-ABL in combination with secondary leukemia-specific pathways in CML cells leads to enhanced apoptosis and decreased proliferation.

Molecular pharmaceutics - 7 Jan 2013

Woessner David W, Lim Carol S

Abstract excerpt

Chronic myeloid leukemia (CML) is a myeloproliferative disorder caused by expression of the fusion gene BCR-ABL following a chromosomal translocation in the hematopoietic stem cell. Therapeutic management of CML uses tyrosine kinase inhibitors (TKIs), which block ABL-signaling and effectively kill peripheral cells with BCR-ABL. However, TKIs are not curative, and chronic use is required in order to treat CML. The...

Read the complete abstract on PubMed

Topics

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

Share to Cell Death
Share to Cell Growth Processes
Share to Fusion Proteins, bcr-abl

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hematopoietic Stem Cells

Share to K562 Cells

Share to Leukemia, Myelogenous, Chronic, BCR-ABL Positive

Share to Mucin-1

Share to Protein-Tyrosine Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 23211037
DOI: 10.1021/mp300405n
PMCID: PMC3604893

Genes

BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Disrupting BCR-ABL in combination with secondary leukemia-specific pathways in CML cells leads to enhanced apoptosis and decreased proliferation.PMID 23211037Read ↗

Multidomain targeting of Bcr-Abl by disruption of oligomerization and tyrosine kinase inhibition: toward eradication of CML.Semantic proximity Read ↗

Secondary fusion proteins as a mechanism of BCR::ABL1 kinase-independent resistance in chronic myeloid leukaemia.Semantic proximity Read ↗

Improved Coiled-Coil Design Enhances Interaction with Bcr-Abl and Induces ApoptosisSemantic proximity Read ↗

Celastrol induces DNA damage and cell death in BCR-ABL T315I-mutant CML by targeting YY1 and HMCES.Semantic proximity Read ↗

Phosphorylation of BECLIN-1 by BCR-ABL suppresses autophagy in chronic myeloid leukemiaSemantic proximity Read ↗

Biological Features of KLC2 Mutations in Chronic Myeloid Leukemia and Their Contribution to Inducing Drug Resistance.Semantic proximity Read ↗

The PIP4K2 inhibitor THZ-P1-2 exhibits antileukemia activity by disruption of mitochondrial homeostasis and autophagySemantic proximity Read ↗

The PIP4K2 inhibitor THZ-P1-2 exhibits antileukemia activity by disruption of mitochondrial homeostasis and autophagySemantic proximity Read ↗

Glucosylceramide synthase inhibitor PDMP sensitizes chronic myeloid leukemia T315I mutant to Bcr-Abl inhibitor and cooperatively induces glycogen synthase kinase-3-regulated apoptosis.Semantic proximity Read ↗

A cell competition-based drug screen identifies a novel compound that induces dual c-Myc depletion and p53 activationSemantic proximity Read ↗

Loss of G0/G1 switch gene 2 (G0S2) promotes disease progression and drug resistance in chronic myeloid leukaemia (CML) by disrupting glycerophospholipid metabolismSemantic proximity Read ↗

Acquired miR-142 deficit in leukemic stem cells suffices to drive chronic myeloid leukemia into blast crisisSemantic proximity Read ↗

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