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

FLT3-ITD and TLR9 use Bruton tyrosine kinase to activate distinct transcriptional programs mediating AML cell survival and proliferation

21 Jan 2015

Abstract excerpt

Acute myeloid leukemia (AML) is driven by niche-derived and cell-autonomous stimuli. Although many cell-autonomous disease drivers are known, niche-dependent signaling in the context of the genetic disease heterogeneity has been difficult to investigate. Here, we analyzed the role of Bruton tyrosine kinase (BTK) in AML. BTK was frequently expressed, and its inhibition strongly impaired the proliferation and...

Read the complete abstract on PubMed

Topics

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

Share to Acute Myeloid Leukemia Research
Share to Chronic Lymphocytic Leukemia Research
Share to Lymphoma Diagnosis and Treatment

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 25605370
DOI: 10.1182/blood-2014-06-585216

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

FLT3-ITD and TLR9 use Bruton tyrosine kinase to activate distinct transcriptional programs mediating AML cell survival and proliferationPMID 25605370Read ↗

A JAK/STAT-Mediated Inflammatory Signaling Cascade Drives Oncogenesis In AF10-Rearranged AMLSemantic proximity Read ↗

Targeting BTK for the treatment of FLT3-ITD mutated acute myeloid leukemia.Semantic proximity Read ↗

Chronic FLT3-ITD Signaling in Acute Myeloid Leukemia Is Connected to a Specific Chromatin Signature.Semantic proximity Read ↗

A JAK/STAT-mediated inflammatory signaling cascade drives oncogenesis in AF10-rearranged AMLSemantic proximity Read ↗

Deciphering the Complexities of Acute Myeloid Leukemia: Emerging Roles of Epithelial to Mesenchymal Transition Transcription Factors (EMT-TFs) in Disease ProgressionSemantic proximity Read ↗

Mutated tyrosine kinases as therapeutic targets in myeloid leukemias.Semantic proximity Read ↗

Differential signaling of Flt3 activating mutations in acute myeloid leukemia: a working model.Semantic proximity Read ↗

Receptor tyrosine kinase alterations in AML - biology and therapy.Semantic proximity Read ↗

The Role of Epithelial-to-Mesenchymal Transition Transcription Factors (EMT-TFs) in Acute Myeloid Leukemia ProgressionSemantic proximity Read ↗

Role of Bruton’s tyrosine kinase in B cells and malignanciesSemantic proximity Read ↗

A distinct core regulatory module enforces oncogene expression in KMT2A-rearranged leukemiaSemantic proximity Read ↗

SYK is a critical regulator of FLT3 in acute myeloid leukemia.Semantic proximity Read ↗

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