Evidence map›Paper›PMID 24608428›Full record

ReviewOncogene2015

Targeting RNA polymerase I to treat MYC-driven cancer.

G Poortinga, L M Quinn, R D Hannan

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  8. Review
  9. The functional GRHL3-filaggrin axis maintains a tumor differentiation potential and influences drug sensitivity.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  10. Targeting cancer via ribosome biogenesis: the cachexia perspective.Cellular and molecular life sciences : CMLS · 2021
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
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  19. Article
  20. Interaction of the oncoprotein transcription factor MYC with its chromatin cofactor WDR5 is essential for tumor maintenance.Proceedings of the National Academy of Sciences of the United States of America · 2019
    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

3 authors at 2 institutions in 1 country.

G Poortinga1] Division of Cancer Research, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Victoria, Australia [3] Department of Medicine, St Vincent's Hospital, University of Melbourne, Fitzroy, Victoria, Australia.
L M QuinnDepartment of Anatomy and Neuroscience, University of Melbourne, Parkville, Victoria, Australia.
R D Hannan1] Division of Cancer Research, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Victoria, Australia [3] Department of Biochemistry and Molecular Biology, University of Melbourne, Melbourne, Victoria, Australia [4] Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, Australia [5] School of Biomedical Sciences, University of Queensland, Brisbane, Queensland, Australia.
Peter MacCallum Cancer Centre · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The MYC oncoprotein and transcription factor is dysregulated in a majority of human cancers and is considered a major driver of the malignant phenotype. As such, developing drugs for effective inhibition of MYC in a manner selective to malignancies is a 'holy grail' of transcription factor-based cancer therapy. Recent advances in elucidating MYC biology in both normal cells and pathological settings were anticipated to bring inhibition of tumorigenic MYC function closer to the clinic. However, while the extensive array of cellular pathways that MYC impacts present numerous fulcrum points on which to leverage MYC's therapeutic potential, identifying the critical target(s) for MYC-specific cancer therapy has been difficult to achieve. Somewhat unexpectedly, MYC's fundamental role in regulating the 'housekeeping' process of ribosome biogenesis, one of the most ubiquitously required and conserved cell functions, may provide the Achilles' heel for therapeutically targeting MYC-driven tumors.

Indexed as

AnimalsHumansNeoplasmsProto-Oncogene Proteins c-mdm2Proto-Oncogene Proteins c-mycRibosomesRNA Polymerase ITumor Suppressor Protein p53Proto-Oncogene Proteins c-mdm2Proto-Oncogene Proteins c-mycRNA Polymerase ITumor Suppressor Protein p53

Identifiers

PMID24608428
OpenAlexW1985122162

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.