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

The menin-MLL1 interaction is a molecular dependency in NUP98-rearranged AML

28 Sept 2021

Abstract excerpt

Translocations involving the NUP98 gene produce NUP98-fusion proteins and are associated with a poor prognosis in acute myeloid leukemia (AML). MLL1 is a molecular dependency in NUP98-fusion leukemia, and therefore we investigated the efficacy of therapeutic blockade of the menin-MLL1 interaction in NUP98-fusion leukemia models. Using mouse leukemia cell lines driven by NUP98-HOXA9 and NUP98-JARID1A fusion...

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 Multiple Myeloma Research and Treatments
Share to Protein Degradation and Inhibitors

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 34582559
DOI: 10.1182/blood.2021012806

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The menin-MLL1 interaction is a molecular dependency in NUP98-rearranged AMLPMID 34582559Read ↗

The MLL–Menin Interaction is a Therapeutic Vulnerability in NUP98-rearranged AMLSemantic proximity Read ↗

CDK6 is an essential direct target of NUP98 fusion proteins in acute myeloid leukemiaSemantic proximity Read ↗

Fusion oncoproteins and cooperating mutations define disease phenotypes in<i>NUP98</i>-rearranged leukemiaSemantic proximity Read ↗

A Molecular Switch between Mammalian MLL Complexes Dictates Response to Menin–MLL InhibitionSemantic proximity Read ↗

NUP98 Rearrangements in AML: Molecular Mechanisms and Clinical ImplicationsSemantic proximity Read ↗

Therapeutic targeting in pediatric acute myeloid leukemia with aberrant HOX/MEIS1 expressionSemantic proximity Read ↗

NUP98 gene fusions and hematopoietic malignancies: common themes and new biologic insightsSemantic proximity Read ↗

Mechanistic insights and potential therapeutic approaches for NUP98 -rearranged hematologic malignanciesSemantic proximity Read ↗

Fusion oncoproteins and cooperating mutations define disease phenotypes in NUP98 -rearranged leukemiaSemantic proximity Read ↗

NUP98-MLL fusion in human acute myeloblastic leukemiaSemantic proximity Read ↗

NUP98 oncofusions in myeloid malignancies: An update on molecular mechanisms and therapeutic opportunitiesSemantic proximity Read ↗

A molecular switch between mammalian MLL complexes dictates response to Menin-MLL inhibitionSemantic proximity Read ↗

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