Evidence map›Paper›PMID 34131281›Full record

ReviewLeukemia2021

Therapeutic implications of menin inhibition in acute leukemias.

Ghayas C Issa, Farhad Ravandi, Courtney D DiNardo, Elias Jabbour, Hagop M Kantarjian, Michael Andreeff

Abstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed
26.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

123 citing papers in PubMed, 184 citations in OpenAlex.

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  2. Ziftomenib in Relapsed or RefractoryJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2025
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63 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Ghayas C IssaDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. gcissa@mdanderson.org.ORCID http://orcid.org/0000-0002-4339-8683
Farhad RavandiDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Courtney D DiNardoDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID http://orcid.org/0000-0001-9003-0390
Elias JabbourDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID http://orcid.org/0000-0003-4465-6119
Hagop M KantarjianDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID http://orcid.org/0000-0002-1908-3307
Michael AndreeffDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. mandreef@mdanderson.org.ORCID http://orcid.org/0000-0002-1144-1958
The University of Texas MD Anderson Cancer Center · US

Funding

Paul Calabresi Clinical Oncology AwardK12CA088084 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI David S. Hong, Scott Kopetz · 2000 to 2026
$14.0M
NCI NIH HHS K12 CA088084
6 · The paper itself

Abstract

Menin inhibitors are novel targeted agents currently in clinical development for the treatment of genetically defined subsets of acute leukemia. Menin has a tumor suppressor function in endocrine glands. Germline mutations in the gene encoding menin cause the multiple endocrine neoplasia type 1 (MEN1) syndrome, a hereditary condition associated with tumors of the endocrine glands. However, menin is also critical for leukemogenesis in subsets driven by rearrangement of the Lysine Methyltransferase 2A (KMT2A) gene, previously known as mixed-lineage leukemia (MLL), which encodes an epigenetic modifier. These seemingly opposing functions of menin can be explained by its various roles in gene regulation. Therefore, leukemias with rearrangement of KMT2A are predicted to respond to menin inhibition with early clinical data validating this proof-of-concept. These leukemias affect infants, children and adults, and lead to adverse outcomes with current standard therapies. Recent studies have identified novel targets in acute leukemia that are susceptible to menin inhibition, such as mutated Nucleophosmin 1 (NPM1), the most common genetic alteration in adult acute myeloid leukemia (AML). In addition to these alterations, other leukemia subsets with similar transcriptional dependency could be targeted through menin inhibition. This led to rationally designed clinical studies, investigating small-molecule oral menin inhibitors in relapsed acute leukemias with promising early results. Herein, we discuss the physiologic and malignant biology of menin, the mechanisms of leukemia in these susceptible subsets, and future therapeutic strategies using these inhibitors in acute leukemia.

Indexed as

Antineoplastic AgentsHumansLeukemia, Myeloid, AcuteMolecular Targeted TherapyNucleophosminProto-Oncogene ProteinsAntineoplastic AgentsMEN1 protein, humanNPM1 protein, humanNucleophosminProto-Oncogene Proteins

Identifiers

PMID34131281
OpenAlexW3167620265

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.