Evidence map›Paper›PMID 24737842›Full record

ReviewCold Spring Harbor perspectives in medicine2014

MYC and the art of microRNA maintenance.

James N Psathas, Andrei Thomas-Tikhonenko

Abstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
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

41 citing papers in PubMed.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Myc beyond Cancer: Regulation of Mammalian Tissue Regeneration.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Review
  8. Review
  9. Review
  10. Review
  11. MYC Hyperactivates Wnt Signaling inMolecular cancer research : MCR · 2021
    Article
  12. Review
  13. RNA-binding proteins of COSMIC importance in cancer.The Journal of clinical investigation · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article
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

2 authors.

James N PsathasDivision of Cancer Pathobiology and Center for Childhood Cancer Research, Children's Hospital of Philadelphia and Department of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104.
Andrei Thomas-TikhonenkoDivision of Cancer Pathobiology and Center for Childhood Cancer Research, Children's Hospital of Philadelphia and Department of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104.

Funding

IMMUNOBIOLOGY OF NORMAL AND NEOPLASTIC LYMPHOCYTEST32CA009140 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Malay Haldar, WARREN S PEAR · 1985 to 2026
$16.1M
Training In Tumor VirologyT32CA115299 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2006 to 2021
$4.7M
Molecular mechanisms of Myc-induced tumor neovascularizationR01CA122334 · NCI · UNIVERSITY OF PENNSYLVANIA · PI THOMAS-TIKHONENKO, ANDREI · 2007 to 2012
$1.5M
NCI NIH HHS CA009140NCI NIH HHS CA115299NCI NIH HHS CA122334NCI NIH HHS R01 CA122334NCI NIH HHS T32 CA009140NCI NIH HHS T32 CA115299
6 · The paper itself

Abstract

MYC is a noncanonical transcription factor that binds to thousands of genomic loci and affects >15% of the human transcriptome, with surprisingly little overlap between MYC-bound and -regulated genes. This discordance raises the question whether MYC chooses its targets based on their individual biological effects ("a la carte") or by virtue of belonging to a certain group of genes (on a "prix fixe" basis). This review presents evidence for a prix fixe, posttranscriptional model whereby MYC initially deregulates a select number of microRNAs. These microRNAs then target a broad spectrum of genes based solely on the presence in their 3' UTRs (untranslated regions) of distinct "seed" sequences. Existing evidence suggests that there are significant microRNA components to all key MYC-driven phenotypes, including cell-cycle progression, apoptosis, metabolism, angiogenesis, metastasis, stemness, and hematopoiesis. Furthermore, each of these cell-intrinsic and -extrinsic phenotypes is likely attributable to deregulation of multiple microRNA targets acting in different, yet frequently overlapping, pathways. The habitual targeting of multiple genes within the same pathway might account for the robustness and persistence of MYC-induced phenotypes.

Indexed as

ApoptosisCell CycleHematopoiesisHumansMicroRNAsMitosisNeovascularization, PhysiologicProto-Oncogene Proteins c-mycStem CellsMicroRNAsProto-Oncogene Proteins c-myc

Identifiers

PMID24737842
PMCPMC4109576

What OpenQuestion holds

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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.