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

Bone marrow stroma-mediated resistance to FLT3 inhibitors in FLT3-ITD AML is mediated by persistent activation of extracellular regulated kinase.

British journal of haematology - 1 Jan 2014

Yang Xiaochuan, Sexauer Amy, Levis Mark

Abstract excerpt

A consistent pattern of response has been observed when FMS-like tyrosine kinase 3 (FLT3) tyrosine kinase inhibitors (TKIs) have been used as monotherapy to treat patients with relapsed or refractory FLT3- internal tandem duplication (ITD) acute myeloid leukaemia (AML). Circulating blasts are cleared from the peripheral blood, while bone marrow blasts are either unaffected or are cleared from the marrow at a much...

Read the complete abstract on PubMed

Topics

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

Share to Bone Marrow Cells
Share to Cell Communication

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Coculture Techniques

Share to Extracellular Signal-Regulated MAP Kinases

Share to fms-Like Tyrosine Kinase 3

Share to Gene Duplication

Share to Leukemia, Myeloid, Acute

Share to Stromal Cells

Source

Open in PubMed Open full text

Identifiers

PMID: 24116827
DOI: 10.1111/bjh.12599
PMCID: PMC4076672

Genes

FLT3

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

Bone marrow stroma-mediated resistance to FLT3 inhibitors in FLT3-ITD AML is mediated by persistent activation of extracellular regulated kinase.PMID 24116827Read ↗

Using combination therapy to override stromal-mediated chemoresistance in mutant FLT3-positive AML: synergism between FLT3 inhibitors, dasatinib/multi-targeted inhibitors and JAK inhibitors.Semantic proximity Read ↗

Selective Akt Inhibitors Synergize with Tyrosine Kinase Inhibitors and Effectively Override Stroma-Associated Cytoprotection of Mutant FLT3-Positive AML CellsSemantic proximity Read ↗

p53 activation of mesenchymal stromal cells partially abrogates microenvironment-mediated resistance to FLT3 inhibition in AML through HIF-1α-mediated down-regulation of CXCL12.Semantic proximity Read ↗

Hematopoietic cytokines mediate resistance to targeted therapy in FLT3-ITD acute myeloid leukemiaSemantic proximity Read ↗

Stromal-mediated protection of tyrosine kinase inhibitor-treated BCR-ABL-expressing leukemia cellsSemantic proximity Read ↗

Mechanisms of apoptosis induction by simultaneous inhibition of PI3K and FLT3-ITD in AML cells in the hypoxic bone marrow microenvironment.Semantic proximity Read ↗

Effects of FLT3 Ligand on Proliferation and Survival of Myeloid Leukemia CellsSemantic proximity Read ↗

Flt3-mediated signaling in human acute myelogenous leukemia (AML) blasts: a functional characterization of Flt3-ligand effects in AML cell populations with and without genetic Flt3 abnormalities.Semantic proximity Read ↗

Targeting the leukemia microenvironment by CXCR4 inhibition overcomes resistance to kinase inhibitors and chemotherapy in AML.Semantic proximity Read ↗

Tyrosine kinase inhibitor insensitivity of non-cycling CD34+ human acute myeloid leukaemia cells with FMS-like tyrosine kinase 3 mutations.Semantic proximity Read ↗

Stroma-supported culture in childhood B-lineage acute lymphoblastic leukemia cells predicts treatment outcome.Semantic proximity Read ↗

Bone marrow-derived stromal cells prevent apoptotic cell death in B- lineage acute lymphoblastic leukemiaSemantic proximity Read ↗

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