Evidence map›Paper›PMID 23097355›Full record

ArticleStem cells (Dayton, Ohio)2013

Fibroblast growth factor receptor signaling is essential for normal mammary gland development and stem cell function.

Adam C Pond, Xue Bin, Torey Batts, Kevin Roarty, Susan Hilsenbeck, Jeffrey M Rosen

Open access · greenAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

63 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
  2. The dynamics of tubulogenesis in development and disease.Development (Cambridge, England) · 2025
    Review
  3. Embryonic Mammary Gland Morphogenesis.Advances in experimental medicine and biology · 2025
    Review
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3 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 1 institution in 1 country.

Adam C PondDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
Xue Bin
Torey Batts
Kevin Roarty
Susan Hilsenbeck
Jeffrey M Rosen
Baylor College of Medicine · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Initiative for Maximizing Student Development (IMSD) ProgramR25GM056929 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI PEREIRA, FRED A · 1998 to 2023
$12.4M
MALAT1 lncRNA as a Therapeutic Target in Triple Negative Breast CancerR01CA016303 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ROSEN, JEFFREY MARK · 1985 to 2022
$8.1M
HORMONAL REGULATION OF BREAST CANCERR37CA016303 · NCI · BAYLOR COLLEGE OF MEDICINE · PI ROSEN, JEFFREY MARK · 1989 to 2011
$7.3M
NCI NIH HHS P30 CA125123NCI NIH HHS P30-CA125123NCI NIH HHS R01 CA016303NCI NIH HHS R37 CA016303NCI NIH HHS R37-CA16303NIGMS NIH HHS R25 GM056929
6 · The paper itself

Abstract

Fibroblast growth factor (FGF) signaling plays an important role in embryonic stem cells and adult tissue homeostasis, but the function of FGFs in mammary gland stem cells is less well defined. Both FGFR1 and FGFR2 are expressed in basal and luminal mammary epithelial cells (MECs), suggesting that together they might play a role in mammary gland development and stem cell dynamics. Previous studies have demonstrated that the deletion of FGFR2 resulted only in transient developmental defects in branching morphogenesis. Using a conditional deletion strategy, we investigated the consequences of FGFR1 deletion alone and then the simultaneous deletion of both FGFR1 and FGFR2 in the mammary epithelium. FGFR1 deletion using a keratin 14 promoter-driven Cre-recombinase resulted in an early, yet transient delay in development. However, no reduction in functional outgrowth potential was observed following limiting dilution transplantation analysis. In contrast, a significant reduction in outgrowth potential was observed upon the deletion of both FGFR1 and FGFR2 in MECs using adenovirus-Cre. Additionally, using a fluorescent reporter mouse model to monitor Cre-mediated recombination, we observed a competitive disadvantage following transplantation of both FGFR1/R2-null MECs, most prominently in the basal epithelial cells. This correlated with the complete loss of the mammary stem cell repopulating population in the FGFR1/R2-attenuated epithelium. FGFR1/R2-null MECs were partially rescued in chimeric outgrowths containing wild-type MECs, suggesting the potential importance of paracrine mechanisms involved in the maintenance of the basal epithelial stem cells. These studies document the requirement for functional FGFR signaling in mammary stem cells during development.

Indexed as

AnimalsEpithelial CellsFemaleGene Knockout TechniquesMammary Glands, AnimalMiceMice, Inbred C57BLMice, TransgenicReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 2Signal TransductionStem CellsFgfr1 protein, mouseFgfr2 protein, mouseReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 2

Identifiers

PMID23097355
PMCPMC3690809
OpenAlexW2062329509

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.