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

A JAK/STAT-mediated inflammatory signaling cascade drives oncogenesis in AF10-rearranged AML

9 Mar 2021

Abstract excerpt

Leukemias bearing fusions of the AF10/MLLT10 gene are associated with poor prognosis, and therapies targeting these fusion proteins (FPs) are lacking. To understand mechanisms underlying AF10 fusion-mediated leukemogenesis, we generated inducible mouse models of acute myeloid leukemia (AML) driven by the most common AF10 FPs, PICALM/CALM-AF10 and KMT2A/MLL-AF10, and performed comprehensive characterization of the...

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 Myeloid Leukemia Treatments
Share to Myeloproliferative Neoplasms: Diagnosis and Treatment

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 33690798
DOI: 10.1182/blood.2020009023

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A JAK/STAT-mediated inflammatory signaling cascade drives oncogenesis in AF10-rearranged AMLPMID 33690798Read ↗

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

The AF10 leucine zipper is required for leukemic transformation of myeloid progenitors by MLL-AF10Semantic proximity Read ↗

Retroviral insertional mutagenesis identifies Zeb2 activation as a novel leukemogenic collaborating event in CALM-AF10 transgenic mice.Semantic proximity Read ↗

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

Evolution of AF6-RAS association and its implications in mixed-lineage leukemiaSemantic proximity Read ↗

Molecular genetics of human leukemias: new insights into therapy.Semantic proximity Read ↗

Molecular analysis of the CALM/AF10 fusion: identical rearrangements in acute myeloid leukemia, acute lymphoblastic leukemia and malignant lymphoma patientsSemantic proximity Read ↗

The target cell of transformation is distinct from the leukemia stem cell in murine CALM/AF10 leukemia models.Semantic proximity Read ↗

Janus Kinases in LeukemiaSemantic proximity Read ↗

Nuclear factor of activated T-cells, NFATC1, governs FLT3ITD-driven hematopoietic stem cell transformation and a poor prognosis in AMLSemantic proximity Read ↗

Mouse models of MLL leukemia: recapitulating the human diseaseSemantic proximity Read ↗

The mll-AF9 gene fusion in mice controls myeloproliferation and specifies acute myeloid leukaemogenesis.Semantic proximity Read ↗

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