Evidence map›Paper›PMID 21295272›Full record

ArticleCell stem cell2011

Genetic predisposition directs breast cancer phenotype by dictating progenitor cell fate.

Theresa A Proia, Patricia J Keller, Piyush B Gupta, Ina Klebba, Ainsley D Jones, Maja Sedic, Hannah Gilmore, Nadine Tung, Stephen P Naber, Stuart Schnitt and 2 more

Abstract read
In one paragraph

Article in Cell stem cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 250 papers.

0numbers the graph read from it
0cells of the map it votes in
250citing papers in PubMed
–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

250 citing papers in PubMed.

  1. Trial
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  13. Mechanisms of Regulation of Cell Fate in Breast Development and Cancer.Advances in experimental medicine and biology · 2025
    Review
  14. The mFrontiers in oncology · 2025
    Article
  15. Article
  16. Review
  17. METTL14 suppresses the expression of YAP1 and the stemness of triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2024
    Article
  18. Article
  19. Review
  20. R-loop functions inProceedings of the National Academy of Sciences of the United States of America · 2024
    Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Theresa A ProiaDepartment of Anatomy & Cellular Biology, Sackler School of Biomedical Research, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111, USA.
Patricia J Keller
Piyush B Gupta
Ina Klebba
Ainsley D Jones
Maja Sedic
Hannah Gilmore
Nadine Tung
Stephen P Naber
Stuart Schnitt
Eric S Lander
Charlotte Kuperwasser

Funding

Mechanisms of estrogen action on bone marrow-derived stem stromal cellsR01CA125554 · NCI · TUFTS UNIVERSITY BOSTON · PI KUPERWASSER, CHARLOTTE · 2007 to 2011
$1.5M
NCI NIH HHS CA125554NCI NIH HHS R01 CA125554
6 · The paper itself

Abstract

Women with inherited mutations in the BRCA1 gene have increased risk of developing breast cancer but also exhibit a predisposition for the development of aggressive basal-like breast tumors. We report here that breast epithelial cells derived from patients harboring deleterious mutations in BRCA1 (BRCA1(mut /+) give rise to tumors with increased basal differentiation relative to cells from BRCA1+/+ patients. Molecular analysis of disease-free breast tissues from BRCA1(mut /+) patients revealed defects in progenitor cell lineage commitment even before cancer incidence. Moreover, we discovered that the transcriptional repressor Slug is an important functional suppressor of human breast progenitor cell lineage commitment and differentiation and that it is aberrantly expressed in BRCA1(mut /+) tissues. Slug expression is necessary for increased basal-like phenotypes prior to and after neoplastic transformation. These findings demonstrate that the genetic background of patient populations, in addition to affecting incidence rates, significantly impacts progenitor cell fate commitment and, therefore, tumor phenotype.

Indexed as

AdultAnimalsBreast NeoplasmsFemaleFlow CytometryGenes, BRCA1Genetic Predisposition to DiseaseHumansImmunohistochemistryMiceMice, SCIDMiddle AgedMolecular Sequence DataPhenotypeReverse Transcriptase Polymerase Chain ReactionSnail Family Transcription FactorsSNAI1 protein, humanSnai2 protein, mouseSnail Family Transcription FactorsTranscription Factors

Identifiers

PMID21295272
PMCPMC3050563

What OpenQuestion holds

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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.