Evidence map›Paper›PMID 26923330›Full record

ReviewOncogene2016

Targeting the RB-E2F pathway in breast cancer.

J Johnson, B Thijssen, U McDermott, M Garnett, L F A Wessels, R Bernards

Open access · bronzeAbstract readReview
In one paragraph

Review in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed, 1 pooled it
17.9field-weighted citation impact, top 1% 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

122 citing papers in PubMed, 1 synthesis or guideline pooled it, 209 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. TP53 mutations and MDM2 polymorphisms in breast and ovarian cancers: amelioration by drugs and natural compounds.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

62 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

6 authors at 2 institutions in 2 countries.

J JohnsonDivision of Molecular Carcinogenesis and Cancer Genomics Netherlands, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
B ThijssenDivision of Molecular Carcinogenesis and Cancer Genomics Netherlands, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
U McDermottWellcome Trust Sanger Institute, Cambridge, UK.
M GarnettWellcome Trust Sanger Institute, Cambridge, UK.
L F A WesselsDivision of Molecular Carcinogenesis and Cancer Genomics Netherlands, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
R BernardsDivision of Molecular Carcinogenesis and Cancer Genomics Netherlands, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0001-8677-3423
The Netherlands Cancer Institute · NLWellcome Sanger Institute · GB

Funding

Wellcome Trust 102696StrattonWellcome Trust 102696STRATTON
6 · The paper itself

Abstract

Mutations of the retinoblastoma tumor-suppressor gene (RB1) or components regulating the CDK-RB-E2F pathway have been identified in nearly every human malignancy. Re-establishing cell cycle control through cyclin-dependent kinase (CDK) inhibition has therefore emerged as an attractive option in the development of targeted cancer therapy. The most successful example of this today is the use of the CDK4/6 inhibitor palbociclib combined with aromatase inhibitors for the treatment of estrogen receptor-positive breast cancers. Multiple studies have demonstrated that the CDK-RB-E2F pathway is critical for the control of cell proliferation. More recently, studies have highlighted additional roles of this pathway, especially E2F transcription factors themselves, in tumor progression, angiogenesis and metastasis. Specific E2Fs also have prognostic value in breast cancer, independent of clinical parameters. We discuss here recent advances in understanding of the RB-E2F pathway in breast cancer. We also discuss the application of genome-wide genetic screening efforts to gain insight into synthetic lethal interactions of CDK4/6 inhibitors in breast cancer for the development of more effective combination therapies.

Indexed as

Aromatase InhibitorsBreast NeoplasmsCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6E2F Transcription FactorsFemaleHumansNeovascularization, PathologicPiperazinesProtein Kinase InhibitorsPyridinesRetinoblastoma Binding ProteinsUbiquitin-Protein LigasesAromatase InhibitorsCDK6 protein, humanCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6E2F Transcription FactorspalbociclibPiperazinesProtein Kinase InhibitorsPyridinesRB1 protein, humanRetinoblastoma Binding ProteinsUbiquitin-Protein Ligases

Identifiers

PMID26923330
PMCPMC4950965
OpenAlexW2291124025

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.