Evidence map›Paper›PMID 19143056›Full record

ReviewNature reviews. Cancer2008

Tailoring to RB: tumour suppressor status and therapeutic response.

Erik S Knudsen, Karen E Knudsen

Abstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
214citing papers in PubMed, 1 pooled it
–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

214 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Metabolic Response to CDK4/6 Inhibition in ER+ Breast Cancer Creates a Therapeutic Vulnerability in Drug-Tolerant Persister Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Lactylation and human disease.Expert reviews in molecular medicine · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Concurrent RB1 Loss and BRCA Deficiency Predicts Enhanced Immunologic Response and Long-term Survival in Tubo-ovarian High-grade Serous Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  18. 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
  19. Review
  20. ER-positive and BRCA2-mutated breast cancer: a literature review.European journal of medical research · 2024
    Review

154 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

2 authors.

Erik S KnudsenDepartment of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. eknudsen@kimmelcancercenter.org
Karen E Knudsen

Funding

Cyclin D1: repercussions of AR control and alternative splicing in prostate canceR01CA099996 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, KAREN E · 2003 to 2013
$2.6M
Endocrine disruptors: AR regulation and prostate cancerR01ES016675 · NIEHS · UNIVERSITY OF CINCINNATI · PI KNUDSEN, KAREN E · 2007 to 2011
$1.9M
Role of BAF57 in AR control and prostate cancer growthR01CA116777 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, KAREN E · 2006 to 2010
$1.3M
BRG1/BRM: role in RB tumor suppressor signalingR01CA104213 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, ERIK · 2004 to 2008
$1.2M
Targeting BRM as novel model of prostate hyperplasiaR21CA121402 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, KAREN E · 2006 to 2007
$321k
NCI NIH HHS CA099996NCI NIH HHS CA104213NCI NIH HHS CA10617NCI NIH HHS CA116777NCI NIH HHS R01 CA099996NCI NIH HHS R01 CA104213NCI NIH HHS R01 CA116777NCI NIH HHS R21 CA121402NIEHS NIH HHS R01 ES016675
6 · The paper itself

Abstract

The retinoblastoma tumour suppressor (RB) is a crucial regulator of cell-cycle progression that is invoked in response to a myriad of anti-mitogenic signals. It has been hypothesized that perturbations of the RB pathway confer a synonymous proliferative advantage to tumour cells; however, recent findings demonstrate context-specific outcomes associated with such lesions. Particularly, loss of RB function is associated with differential response to wide-ranging therapeutic agents. Thus, the status of this tumour suppressor may be particularly informative in directing treatment regimens.

Indexed as

AnimalsAntineoplastic AgentsBiomarkersCell CycleCell DeathE2F Transcription FactorsGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansMiceNeoplasmsNeoplasms, Hormone-DependentOrgan SpecificityProtein Kinase InhibitorsRetinoblastoma ProteinSignal TransductionAntineoplastic AgentsBiomarkersE2F Transcription FactorsProtein Kinase InhibitorsRetinoblastoma Protein

Identifiers

PMID19143056
PMCPMC2914856

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.