Evidence map›Paper›PMID 38238471›Full record

ReviewNature reviews. Cancer2024

Linking cell mechanical memory and cancer metastasis.

Elena Cambria, Mark F Coughlin, Marie A Floryan, Giovanni S Offeddu, Sarah E Shelton, Roger D Kamm

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
48.9field-weighted citation impact, top 1% 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

112 citing papers in PubMed, 151 citations in OpenAlex.

  1. Review
  2. Article
  3. Mechanical regulation of cell memory.Nature structural & molecular biology · 2026
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  19. [Research advances of magnetic resonance elastography for assessing the bioinvasiveness in hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Review
  20. Article

52 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 2 institutions in 1 country.

Elena CambriaDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA. ecambria@mit.edu.ORCID http://orcid.org/0000-0001-6896-5421
Mark F CoughlinDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Marie A FloryanDepartment of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Giovanni S OffedduDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Sarah E SheltonDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID http://orcid.org/0000-0002-9358-058X
Roger D KammDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA. rdkamm@mit.edu.ORCID http://orcid.org/0000-0002-7232-304X
Massachusetts Institute of Technology · USDana-Farber Cancer Institute · US

Funding

Studying E-cadherin dynamics during extravasation and metastatic colonizationU54CA261694 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ROGER D KAMM, Vivek Shenoy · 2021 to 2026
$9.1M
Imaging Cancer Angiogenesis with Acoustic Angiography UltrasoundK00CA212227 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SHELTON, SARAH ELIZABETH · 2018 to 2021
$392k
NCI NIH HHS K00 CA212227NCI NIH HHS U54 CA261694
6 · The paper itself

Abstract

Metastasis causes most cancer-related deaths; however, the efficacy of anti-metastatic drugs is limited by incomplete understanding of the biological mechanisms that drive metastasis. Focusing on the mechanics of metastasis, we propose that the ability of tumour cells to survive the metastatic process is enhanced by mechanical stresses in the primary tumour microenvironment that select for well-adapted cells. In this Perspective, we suggest that biophysical adaptations favourable for metastasis are retained via mechanical memory, such that the extent of memory is influenced by both the magnitude and duration of the mechanical stress. Among the mechanical cues present in the primary tumour microenvironment, we focus on high matrix stiffness to illustrate how it alters tumour cell proliferation, survival, secretion of molecular factors, force generation, deformability, migration and invasion. We particularly centre our discussion on potential mechanisms of mechanical memory formation and retention via mechanotransduction and persistent epigenetic changes. Indeed, we propose that the biophysical adaptations that are induced by this process are retained throughout the metastatic process to improve tumour cell extravasation, survival and colonization in the distant organ. Deciphering mechanical memory mechanisms will be key to discovering a new class of anti-metastatic drugs.

Indexed as

Mechanotransduction, CellularNeoplasmsCell MovementCell ProliferationEpigenesis, GeneticHumansNeoplasm MetastasisTumor Microenvironment

Identifiers

PMID38238471
PMCPMC11146605
OpenAlexW4390986522

What OpenQuestion holds

Textmetadata
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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.