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

Enhanced ABL-inhibitor-induced MAPK-activation in T315I-BCR-ABL-expressing cells: a potential mechanism of altered leukemogenicity.

Journal of cancer research and clinical oncology - 1 Feb 2012

Härtel Nicolai, Klag Thomas, Hanfstein Benjamin, Mueller Martin C, Schenk Thomas, Erben Philipp, Hochhaus Andreas, La Rosée Paul

Abstract excerpt

BACKGROUND: Targeted treatment of chronic myelogenous leukemia using imatinib has dramatically improved patient outcome. However, residual disease can be detected in the majority of patients treated with imatinib. Compensatory activation of MAP kinases (MAPK1/2) in response to BCR-ABL-inhibitors has been reported as a potential cytokine-dependent resistance mechanism leading to the rescue of leukemic progenitor...

Read the complete abstract on PubMed

Topics

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

Share to Antigens, CD34
Share to Dasatinib

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

Share to Interleukin-3

Share to Mitogen-Activated Protein Kinase Kinases

Share to Myeloid Cells

Share to src-Family Kinases

Share to Thiazoles

Source

Identifiers

PMID: 22089930
DOI: 10.1007/s00432-011-1086-x

Genes

BCR
SRC
MAPK1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Enhanced ABL-inhibitor-induced MAPK-activation in T315I-BCR-ABL-expressing cells: a potential mechanism of altered leukemogenicity.PMID 22089930Read ↗

Activation of the p38 Map kinase pathway is essential for the antileukemic effects of dasatinib.Semantic proximity Read ↗

<i>ABL</i> Oncogenes and Phosphoinositide 3-Kinase: Mechanism of Activation and Downstream EffectorsSemantic proximity Read ↗

Targeting mutated protein tyrosine kinases and their signaling pathways in hematologic malignancies.Semantic proximity Read ↗

NF-kappaB inhibition triggers death of imatinib-sensitive and imatinib-resistant chronic myeloid leukemia cells including T315I Bcr-Abl mutants.Semantic proximity Read ↗

Capitalizing on paradoxical activation of the mitogen-activated protein kinase pathway for treatment of Imatinib-resistant mast cell leukemia.Semantic proximity Read ↗

The Bcr-Abl mutations T315I and Y253H do not confer a growth advantage in the absence of imatinib.Semantic proximity Read ↗

MEK-Dependent Negative Feedback Underlies BCR–ABL-Mediated Oncogene AddictionSemantic proximity Read ↗

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

ERK2, but Not ERK1, Mediates Acquired and “De novo” Resistance to Imatinib Mesylate: Implication for CML TherapySemantic proximity Read ↗

Enhanced MAPK signaling induced by CSF3R mutants confers dependence to DUSP1 for leukemic transformation.Semantic proximity Read ↗

Two Transforming C-RAF Germ-Line Mutations Identified in Patients with Therapy-Related Acute Myeloid LeukemiaSemantic proximity Read ↗

Adaptive phenotypic modulations lead to therapy resistance in chronic myeloid leukemia cells.Semantic proximity Read ↗

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