Evidence map›Paper›PMID 33037194›Full record

ReviewNature communications2020

Concepts of extracellular matrix remodelling in tumour progression and metastasis.

Juliane Winkler, Abisola Abisoye-Ogunniyan, Kevin J Metcalf, Zena Werb

Abstract readReview
In one paragraph

Review in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,341 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,341citing papers in PubMed, 1 pooled it
–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

1,341 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Understanding and targeting the tumour matrisome.Nature reviews. Clinical oncology · 2026
    Review
  10. Review
  11. Review
  12. Biomimetic Scaffold-Based 3D Models for Decoding Cancer Biology and Advancing Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

1,281 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

4 authors.

Juliane Winkler *Department of Anatomy, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, 94143, USA. juliane.winkler@ucsf.edu.ORCID http://orcid.org/0000-0002-9762-1721
Abisola Abisoye-Ogunniyan *Department of Anatomy, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, 94143, USA.ORCID http://orcid.org/0000-0002-8646-9031
Kevin J MetcalfDepartment of Anatomy, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, 94143, USA.ORCID http://orcid.org/0000-0002-2721-3378
Zena WerbDepartment of Anatomy, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, 94143, USA.ORCID http://orcid.org/0000-0002-6525-3872

Funding

Molecular and Cellular Mechanisms in CancerT32CA108462 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GOGA, ANDREI · 2004 to 2024
$10.4M
Integrative approach to heterogeneity in breast cancer metastasisU01CA199315 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GOGA, ANDREI, SPELLMAN, PAUL T. · 2016 to 2020
$3.2M
Role of GATA3 in transcriptional pathways suppressing breast cancer metastasisR01CA190851 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WERB, ZENA · 2015 to 2019
$2.0M
Inter-regulatory function of immune-modulation and angiogenesis in cancerR01CA201537 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BERGERS, GABRIELE · 2016 to 2020
$1.7M
NCI NIH HHS R01 CA190851NCI NIH HHS R01 CA201537NCI NIH HHS T32 CA108462NCI NIH HHS U01 CA199315
6 · The paper itself

Abstract

Tissues are dynamically shaped by bidirectional communication between resident cells and the extracellular matrix (ECM) through cell-matrix interactions and ECM remodelling. Tumours leverage ECM remodelling to create a microenvironment that promotes tumourigenesis and metastasis. In this review, we focus on how tumour and tumour-associated stromal cells deposit, biochemically and biophysically modify, and degrade tumour-associated ECM. These tumour-driven changes support tumour growth, increase migration of tumour cells, and remodel the ECM in distant organs to allow for metastatic progression. A better understanding of the underlying mechanisms of tumourigenic ECM remodelling is crucial for developing therapeutic treatments for patients.

Indexed as

AnimalsCell Transformation, NeoplasticExtracellular MatrixHumansNeoplasmsTumor Microenvironment

Identifiers

PMID33037194
PMCPMC7547708

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.