Evidence map›Paper›PMID 29692417›Full record

ReviewNature reviews. Cancer2018

Non-canonical functions of the RB protein in cancer.

Frederick A Dick, David W Goodrich, Julien Sage, Nicholas J Dyson

Abstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

107 citing papers in PubMed, 171 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Disruption Events in the HPV18International journal of molecular sciences · 2025
    Article
  7. Article
  8. Proteogenomic discovery ofScience advances · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. APC/C prevents a noncanonical order of cyclin/CDK activity to maintain CDK4/6 inhibitor-induced arrest.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. EHMT2-mediated transcriptional reprogramming drives neuroendocrine transformation in non-small cell lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

47 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

4 authors at 4 institutions in 2 countries.

Frederick A DickLondon Regional Cancer Program, Children's Health Research Institute, Western University, London, Ontario, Canada. fdick@uwo.ca.
David W GoodrichDepartment of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY, USA.
Julien SageDepartments of Pediatrics and Genetics, Stanford University, Stanford, CA, USA.ORCID http://orcid.org/0000-0002-8928-9968
Nicholas J DysonMassachusetts General Hospital Cancer Center, Laboratory of Molecular Oncology, Harvard Medical School, Charlestown, MA, USA.
Harvard University · USPediatrics and Genetics · USRoswell Park Comprehensive Cancer Center · USWestern University · CA

Funding

The RB pathway in liver cancerR01CA114102 · NCI · STANFORD UNIVERSITY · PI SAGE, JULIEN · 2006 to 2016
$2.9M
Exploiting RB1 deficiency for the treatment of lethal neuroendocrine prostate cancerR01CA207757 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI ELLIS, LEIGH, GOODRICH, DAVID W. · 2016 to 2020
$2.8M
The consequences of RB-lossR01GM117413 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 2016 to 2019
$2.1M
Chromatin changes in the thymus epithelium during agingR21AG050296 · NIA · STANFORD UNIVERSITY · PI SAGE, JULIEN · 2016 to 2017
$460k
(PQB5) Does the timing of Pten and Rb1 mutation affect prostate cancer phenotypesR21CA179907 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI GOODRICH, DAVID W. · 2013 to 2014
$401k
NCI NIH HHS R01 CA114102NCI NIH HHS R01 CA207757NCI NIH HHS R21 CA179907NIA NIH HHS R21 AG050296NIGMS NIH HHS R01 GM117413
6 · The paper itself

Abstract

The canonical model of RB-mediated tumour suppression developed over the past 30 years is based on the regulation of E2F transcription factors to restrict cell cycle progression. Several additional functions have been proposed for RB, on the basis of which a non-canonical RB pathway can be described. Mechanistically, the non-canonical RB pathway promotes histone modification and regulates chromosome structure in a manner distinct from cell cycle regulation. These functions have implications for chemotherapy response and resistance to targeted anticancer agents. This Opinion offers a framework to guide future studies of RB in basic and clinical research.

Indexed as

Chromosome StructuresDrug Resistance, NeoplasmHistone CodeAntineoplastic AgentsCell ProliferationChromatinDNA RepairE2F Transcription FactorsEpigenesis, GeneticGenomic InstabilityHumansMolecular Targeted TherapyNeoplasmsPhosphorylationRetinoblastoma ProteinAntineoplastic AgentsChromatinE2F Transcription FactorsRetinoblastoma Protein

Identifiers

PMID29692417
PMCPMC6693677
OpenAlexW2800660846

What OpenQuestion holds

Textmetadata
LicenceTDM
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.