Evidence map›Paper›PMID 32183947›Full record

ArticleCancer cell2020

It's All About MEis: Menin-MLL Inhibition Eradicates NPM1-Mutated and MLL-Rearranged Acute Leukemias in Mice.

Michael C Gundry, Margaret A Goodell, Lorenzo Brunetti

Open access · bronzeAbstract readComment
PubMed Publisher
In one paragraph

Article in Cancer cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Regulation of HOX gene expression in AML.Blood cancer journal · 2024
    Review
  7. Article
  8. Targeting the undruggable: menin inhibitors ante portas.Journal of cancer research and clinical oncology · 2023
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Significance of NPM1 Gene Mutations in AML.International journal of molecular sciences · 2021
    Review
  16. MEIS1 and its potential as a cancer therapeutic target (Review).International journal of molecular medicine · 2021
    Review
  17. Treatment of AML Relapse After Allo-HCT.Frontiers in oncology · 2021
    Review
  18. Review
  19. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Michael C GundryMolecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Margaret A GoodellMolecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA; Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA; Center for Cell and Gene Therapy, Baylor College of Medicine, Houston, TX, USA; Stem Cell and Regenerative Medicine, Baylor College of Medicine, Houston, TX, USA.
Lorenzo BrunettiDepartment of Medicine, University of Perugia, Perugia, Italy. Electronic address: lorenzo.brunetti@unipg.it.
Baylor College of Medicine · USUniversity of Perugia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several acute myeloid leukemia genetic sub-types converge on high expression of HOX genes, critical for their self-renewal. A new orally bioavailable Menin-MLL inhibitor (VTP-50469) appears to promote their differentiation through direct effects on the HOX cofactor MEIS1, paving the way for clinical trials.

Indexed as

AnimalsChromatinHistone-Lysine N-MethyltransferaseHomeodomain ProteinsMiceMyeloid-Lymphoid Leukemia ProteinNuclear ProteinsNucleophosminChromatinHistone-Lysine N-MethyltransferaseHomeodomain ProteinsMyeloid-Lymphoid Leukemia ProteinNPM1 protein, humanNpm1 protein, mouseNuclear ProteinsNucleophosmin

Identifiers

PMID32183947
OpenAlexW3011384934

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.