Evidence map›Paper›PMID 31867279›Full record

ReviewFrontiers in oncology2019

The Extracellular, Cellular, and Nuclear Stiffness, a Trinity in the Cancer Resistome-A Review.

Sara Sofia Deville, Nils Cordes

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing 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

67 citing papers in PubMed.

  1. Beyond DNA damage: 3D tumor models and the integrin mechanobiology of radioresistance.Journal of experimental & clinical cancer research : CR · 2026
    Review
  2. Article
  3. Review
  4. The importance of mechanical forces in chronic respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  5. Article
  6. Review
  7. Nuclear destabilisation - a possible genesis of cancer?Biological reviews of the Cambridge Philosophical Society · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Emerin expression stratification across breast cancer subtypes.Cancer treatment and research communications · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. YAP/TAZ drives Notch and angiogenesis mechanoregulation in silico.NPJ systems biology and applications · 2024
    Article
  18. Article
  19. Review
  20. Emerin deficiency drives MCF7 cells to an invasive phenotype.bioRxiv : the preprint server for biology · 2024
    Article

7 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

2 authors.

Sara Sofia DevilleOncoRay - National Center for Radiation Research in Oncology, Faculty of Medicine and University Hospital Carl Gustav Carus, Helmholtz-Zentrum Dresden - Rossendorf, Technische Universität Dresden, Dresden, Germany.
Nils CordesOncoRay - National Center for Radiation Research in Oncology, Faculty of Medicine and University Hospital Carl Gustav Carus, Helmholtz-Zentrum Dresden - Rossendorf, Technische Universität Dresden, Dresden, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alterations in mechano-physiological properties of a tissue instigate cancer burdens in parallel to common genetic and epigenetic alterations. The chronological and mechanistic interrelation between the various extra- and intracellular aspects remains largely elusive. Mechano-physiologically, integrins and other cell adhesion molecules present the main mediators for transferring and distributing forces between cells and the extracellular matrix (ECM). These cues are channeled via focal adhesion proteins, termed the focal adhesomes, to cytoskeleton and nucleus and vice versa thereby affecting the pathophysiology of multicellular cancer tissues. In combination with simultaneous activation of diverse downstream signaling pathways, the phenotypes of cancer cells are created and driven characterized by deregulated transcriptional and biochemical cues that elicit the hallmarks of cancer. It, however, remains unclear how elastostatic modifications, i.e., stiffness, in the extracellular, intracellular, and nuclear compartment contribute and control the resistance of cancer cells to therapy. In this review, we discuss how stiffness of unique tumor components dictates therapy response and what is known about the underlying molecular mechanisms.

Indexed as

cancer resistomecell-extracellular matrix interactionextracellular matrixfocal adhesionsradio(chemo)resistancesolid stressstiffness

Identifiers

PMID31867279
PMCPMC6908495

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.