Evidence map›Paper›PMID 31978211›Full record

ArticleBlood2020

Development and survival of MYC-driven lymphomas require the MYC antagonist MNT to curb MYC-induced apoptosis.

Hai Vu Nguyen, Cassandra J Vandenberg, Ashley P Ng, Mikara R Robati, Natasha S Anstee, Joel Rimes, Edwin D Hawkins, Suzanne Cory

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. MondoA mediates transcriptional coordination between the MYC network and the integrated stress response in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
  4. MNT: a new target for AML.Blood neoplasia · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Demystifying the Druggability of the MYC Family of Oncogenes.Journal of the American Chemical Society · 2023
    Review
  14. BCL-2 protein family: attractive targets for cancer therapy.Apoptosis : an international journal on programmed cell death · 2023
    Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Hai Vu NguyenThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; and.
Cassandra J VandenbergThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; and.
Ashley P NgThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; and.
Mikara R RobatiThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; and.
Natasha S AnsteeThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; and.
Joel RimesThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; and.
Edwin D HawkinsThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; and.
Suzanne CoryThe Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia; and.
The University of Melbourne · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulated overexpression of MYC is implicated in the development and malignant progression of most (∼70%) human tumors. MYC drives cell growth and proliferation, but also, at high levels, promotes apoptosis. Here, we report that the proliferative capacity of MYC-driven normal and neoplastic B lymphoid cells depends on MNT, a MYC-related transcriptional repressor. Our genetic data establish that MNT synergizes with MYC by suppressing MYC-driven apoptosis, and that it does so primarily by reducing the level of pro-apoptotic BIM. In Eμ-Myc mice, which model the MYC/IGH chromosome translocation in Burkitt's lymphoma, homozygous Mnt deletion greatly reduced lymphoma incidence by enhancing apoptosis and markedly decreasing premalignant B lymphoid cell populations. Strikingly, by inducing Mnt deletion within transplanted fully malignant Eμ-Myc lymphoma cells, we significantly extended transplant recipient survival. The dependency of lymphomas on MNT for survival suggests that drugs inhibiting MNT could significantly boost therapy of MYC-driven tumors by enhancing intrinsic MYC-driven apoptosis.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBone MarrowCell Line, TumorCell Transformation, NeoplasticDisease Models, AnimalGene DeletionGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateLymphomaLymphoma, B-CellMiceMice, TransgenicAntineoplastic AgentsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMnt protein, mouseProto-Oncogene Proteins c-mycRepressor Proteins

Identifiers

PMID31978211
PMCPMC7118401
OpenAlexW3001147945

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.