Evidence map›Paper›PMID 21822945›Full record

ReviewJournal of mammary gland biology and neoplasia2011

Mechanisms by which the extracellular matrix and integrin signaling act to regulate the switch between tumor suppression and tumor promotion.

Patricia J Keely

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of mammary gland biology and neoplasia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
6.6field-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

100 citing papers in PubMed, 158 citations in OpenAlex.

  1. Sulindac, a Nonselective NSAID, Reduces Breast Density in Postmenopausal Women with Breast Cancer Treated with Aromatase Inhibitors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
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  19. CSK-mediated signalling by integrins in cancer.Frontiers in cell and developmental biology · 2023
    Review
  20. Article

40 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

1 author at 1 institution in 1 country.

Patricia J KeelyDepartment of Cell and Regenerative Biology, Laboratory for Cellular and Molecular Biology, & Laboratory for Optical and Computational Instrumentation, University of Wisconsin, 227D Bock Laboratories, 1525 Linden Drive, Madison, WI 53706, USA. pjkeely@wisc.edu
University of Wisconsin–Madison · US

Funding

Mechanisms Of Cell Migration On 3D Aligned MatricesR01CA142833 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI FRIEDL, ANDREAS, HAHN, KLAUS M. · 2010 to 2020
$3.4M
Biophysical Regulation of Breast DifferentiationR01CA114462 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI KEELY, PATRICIA J · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA114462NCI NIH HHS R01 CA142833
6 · The paper itself

Abstract

Cell adhesion to the extracellular matrix (ECM) is necessary for development of the mammary gland, and to maintain the normal architecture and function of the gland. Cells adhere to the ECM via the integrin family of trans-membrane receptors, which signal to control mammary-specific gene expression and regulate cell proliferation and survival. During tumor formation, the ECM is extensively remodeled and signaling through integrins is altered such that cells become proliferative and invasive. A key regulator of whether integrin-mediated adhesion will promote tumor suppression or tumor formation is the stiffness of the stromal ECM. The normal mammary gland is typically surrounded by a loose collagenous stroma. An increase in the deposition of collagen and other stromal components is associated with mammographic density, which is one of the greatest risk factors for developing breast carcinoma. Several groups have demonstrated that increased stromal ECM density results in a matrix that is stiffer. Cells sense the stiffness of their surrounding ECM by Rho-mediated contraction of the actin-myosin cytoskeleton. If the surrounding ECM is stiffer than the cell's ability to contract it, then the tensile forces that result are able to drive the clustering of integrins and assemble adhesion signaling complexes. The result is subsequent activation of signaling pathways including FAK, ERK, and PI3K that drive cell proliferation and survival. In contrast, focal complexes are not formed in a compliant matrix, and activation of FAK and pERK is diminished, resulting in control of proliferation. Signaling from FAK moreover regulates p53 and miR-200 members, which control apoptosis and epithelial phenotype, such that a compliant matrix is predicted to promote normal mammary gland architecture and suppress tumor formation.

Indexed as

AnimalsBreast NeoplasmsExtracellular MatrixFemaleHumansIntegrinsMammary Glands, HumanSignal TransductionIntegrins

Identifiers

PMID21822945
PMCPMC3885166
OpenAlexW2039430052

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.