Evidence map›Paper›PMID 35013601›Full record

ReviewNature reviews. Cancer2022

Towards targeting of shared mechanisms of cancer metastasis and therapy resistance.

Felix Weiss, Douglas Lauffenburger, Peter Friedl

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
169citing papers in PubMed, 1 pooled it
27.0field-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

169 citing papers in PubMed, 1 synthesis or guideline pooled it, 271 citations in OpenAlex.

  1. Pooled it
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109 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 3 institutions in 2 countries.

Felix WeissDepartment of Cell Biology, RIMLS, Radboud University Medical Center, Nijmegen, Netherlands.
Douglas LauffenburgerKoch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0000-0002-0050-989X
Peter FriedlDepartment of Cell Biology, RIMLS, Radboud University Medical Center, Nijmegen, Netherlands. peter.friedl@radboudumc.nl.
Massachusetts Institute of Technology · USRadboud University Nijmegen · NLThe University of Texas MD Anderson Cancer Center · US

Funding

Project 3: Physical and Metabolic Constraints of Cancer Cell InvasionU54CA210184 · NCI · CORNELL UNIVERSITY · PI CANTLEY, LEWIS C., FISCHBACH, CLAUDIA · 2016 to 2020
$10.2M
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
European Research Council 617430NCI NIH HHS U54 CA210184NCI NIH HHS U54 CA261694
6 · The paper itself

Abstract

Resistance to therapeutic treatment and metastatic progression jointly determine a fatal outcome of cancer. Cancer metastasis and therapeutic resistance are traditionally studied as separate fields using non-overlapping strategies. However, emerging evidence, including from in vivo imaging and in vitro organotypic culture, now suggests that both programmes cooperate and reinforce each other in the invasion niche and persist upon metastatic evasion. As a consequence, cancer cell subpopulations exhibiting metastatic invasion undergo multistep reprogramming that - beyond migration signalling - supports repair programmes, anti-apoptosis processes, metabolic adaptation, stemness and survival. Shared metastasis and therapy resistance signalling are mediated by multiple mechanisms, such as engagement of integrins and other context receptors, cell-cell communication, stress responses and metabolic reprogramming, which cooperate with effects elicited by autocrine and paracrine chemokine and growth factor cues present in the activated tumour microenvironment. These signals empower metastatic cells to cope with therapeutic assault and survive. Identifying nodes shared in metastasis and therapy resistance signalling networks should offer new opportunities to improve anticancer therapy beyond current strategies, to eliminate both nodular lesions and cells in metastatic transit.

Indexed as

NeoplasmsTumor MicroenvironmentCell CommunicationHumansIntegrinsNeoplasm MetastasisSignal TransductionIntegrins

Identifiers

PMID35013601
PMCPMC10399972
OpenAlexW4206722756

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.