Evidence map›Paper›PMID 20948315›Full record

ArticleCell cycle (Georgetown, Tex.)2010

RB-pathway disruption in breast cancer: differential association with disease subtypes, disease-specific prognosis and therapeutic response.

Adam Ertel, Jeffry L Dean, Hallgeir Rui, Chengbao Liu, Agnes K Witkiewicz, Karen E Knudsen, Erik S Knudsen

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 1 pooled it
7.3field-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

123 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  7. Review
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  13. Proteogenomic discovery ofScience advances · 2025
    Article
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  15. Thymopoietin-The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2025
    Article
  16. Article
  17. Review
  18. Article
  19. Rb Tumor Suppressor in Small Cell Lung Cancer: Combined Genomic and IHC Analysis with a Description of a Distinct Rb-Proficient Subset.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  20. Article

63 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 1 country.

Adam ErtelKimmel Cancer Center, Department of Cancer Biology, Thomas Jefferson University, Philadelphia, PA, USA. aertel@KimmelCancerCenter.org
Jeffry L Dean
Hallgeir Rui
Chengbao Liu
Agnes K Witkiewicz
Karen E Knudsen
Erik S Knudsen
Philadelphia University · USSidney Kimmel Cancer Center · USThomas Jefferson University · USUniversity of Cincinnati · USUniversity of Cincinnati Medical Center · US

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
Experimental Modeling of Human Breast Cancer in MiceR01CA118740 · NCI · THOMAS JEFFERSON UNIVERSITY · PI RUI, HALLGEIR · 2008 to 2012
$1.8M
Action of RB Pathway in Breast Cancer TherapyR01CA129134 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI KNUDSEN, ERIK · 2010 to 2014
$1.7M
NCI NIH HHS CA118740NCI NIH HHS CA129134NCI NIH HHS R01 CA099996NCI NIH HHS R01 CA118740NCI NIH HHS R01 CA129134
6 · The paper itself

Abstract

In breast cancer, inactivation of the RB tumor suppressor gene is believed to occur via multiple mechanisms to facilitate tumorigenesis. However, the prognostic and predictive value of RB status in disease-specific clinical outcomes has remained uncertain. We investigated RB pathway deregulation in the context of both ER-positive and ER-negative disease using combined microarray datasets encompassing over 900 breast cancer patient samples. Disease-specific characteristics of RB pathway deregulation were investigated in this dataset by evaluating correlation among pathway genes as well as differential expression across patient tumor populations defined by ER status. Survival analysis among these breast cancer samples demonstrates that the RB-loss signature is associated with poor disease outcome within several independent cohorts. Within the ER-negative subpopulation, the RB-loss signature is associated with improved response to chemotherapy and longer relapse-free survival. Additionally, while individual genes in the RB target signature closely reproduce its prognostic value, they also serve to predict and monitor response to therapeutic compounds, such as the cytostatic agent PD-0332991. These results indicate that the RB-loss signature expression is associated with poor outcome in breast cancer, but predicts improved response to chemotherapy based on data in ER-negative populations. While the RB-loss signature, as a whole, demonstrates prognostic and predictive utility, a small subset of markers could be sufficient to stratify patients based on RB function and inform the selection of appropriate therapeutic regimens.

Indexed as

Antineoplastic AgentsBreast NeoplasmsDatabases, GeneticDisease-Free SurvivalFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansOligonucleotide Array Sequence AnalysisPrognosisReceptors, EstrogenRetinoblastoma ProteinSignal TransductionTreatment OutcomeAntineoplastic AgentsReceptors, EstrogenRetinoblastoma Protein

Identifiers

PMID20948315
PMCPMC3055199
OpenAlexW2055164947

What OpenQuestion holds

Textmetadata
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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.