Evidence map›Paper›PMID 27914000›Full record

ArticleCancer metastasis reviews2016

From transformation to metastasis: deconstructing the extracellular matrix in breast cancer.

Shelly Kaushik, Michael W Pickup, Valerie M Weaver

Open access · greenAbstract read
In one paragraph

Article in Cancer metastasis reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
7.2field-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

103 citing papers in PubMed, 160 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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  17. The Hippo Pathway in Breast Cancer: The Extracellular Matrix and Hypoxia.International journal of molecular sciences · 2024
    Review
  18. Article
  19. Article
  20. Article

43 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

3 authors at 1 institution in 1 country.

Shelly KaushikCenter for Bioengineering and Tissue Regeneration, Department of Surgery, UCSF, San Francisco, CA, USA.
Michael W PickupCenter for Bioengineering and Tissue Regeneration, Department of Surgery, UCSF, San Francisco, CA, USA.
Valerie M WeaverCenter for Bioengineering and Tissue Regeneration, Department of Surgery, UCSF, San Francisco, CA, USA. Valerie.Weaver@ucsf.edu.
University of California, San Francisco · US

Funding

Molecular and Cellular Mechanisms in CancerT32CA108462 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GOGA, ANDREI · 2004 to 2024
$10.4M
Project 3: Physical and Metabolic Constraints of Cancer Cell InvasionU54CA210184 · NCI · CORNELL UNIVERSITY · PI SCHAFFER, CHRIS B · 2016 to 2020
$10.2M
TGF BETA SUPPRESSION AND PROMOTION OF MAMMARY CARCINOMASR01CA085492 · NCI · VANDERBILT UNIVERSITY · PI MOSES, HAROLD L, WEAVER, VALERIE MARIE · 2000 to 2015
$6.4M
ECM geometrical and mechanical properties modulate RTK signalingU01CA202241 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI GROVES, JAY T., WEAVER, VALERIE MARIE · 2015 to 2019
$3.3M
A biophysical stromal basis for radiation sensitivity in ductal carcinoma in situR01CA174929 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PARK, CATHERINE C, WEAVER, VALERIE MARIE · 2014 to 2018
$3.1M
Tension-Stat3-miR-mediated metastasisR01CA192914 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SEEWALDT, VICTORIA L., WEAVER, VALERIE MARIE · 2015 to 2019
$2.9M
Collagen remodeling and tumor progressionR01CA138818 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WEAVER, VALERIE MARIE · 2010 to 2014
$2.0M
NFkB, tissue polarity and apoptosis resistanceR01CA078731 · NCI · UNIVERSITY OF PENNSYLVANIA · PI WEAVER, VALERIE MARIE · 2000 to 2008
$1.9M
NCI NIH HHS R01 CA078731NCI NIH HHS R01 CA085492NCI NIH HHS R01 CA138818NCI NIH HHS R01 CA174929NCI NIH HHS R01 CA192914NCI NIH HHS T32 CA108462NCI NIH HHS U01 CA202241NCI NIH HHS U54 CA210184
6 · The paper itself

Abstract

The extracellular matrix (ECM) is a guiding force that regulates various developmental stages of the breast. In addition to providing structural support for the cells, it mediates epithelial-stromal communication and provides cues for cell survival, proliferation, and differentiation. Perturbations in ECM architecture profoundly influence breast tumor progression and metastasis. Understanding how a dysregulated ECM can facilitate malignant transformation is crucial to designing treatments to effectively target the tumor microenvironment. Here, we address the contribution of ECM mechanics to breast cancer progression, metastasis, and treatment resistance and discuss potential therapeutic strategies targeting the ECM.

Indexed as

AnimalsBreast NeoplasmsCell Transformation, NeoplasticExtracellular MatrixHumansMammary Neoplasms, ExperimentalNeoplasm MetastasisBreast cancerDesmoplasiaExtracellular matrix (ECM)MechanosignalingMetastasisTreatment resistance

Identifiers

PMID27914000
PMCPMC5215979
OpenAlexW2558180135

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.