Evidence map›Paper›PMID 27854331›Full record

ReviewInternational journal of molecular sciences2016

Tension in Cancer.

Stefanie Löffek, Claus-Werner Franzke, Iris Helfrich

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Effect of hydrogel stiffness on morphology and gene expression pattern of CD44International journal of clinical and experimental pathology · 2019
    Article
  8. Article
  9. Review
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 1 country.

Stefanie LöffekSkin Cancer Unit of the Dermatology Department, Medical Faculty, West German Cancer Center, University Duisburg-Essen, 45147 Essen, Germany. stefanie.loeffek@uk-essen.de.
Claus-Werner FranzkeDepartment of Dermatology and Venerology, Medical Center, University of Freiburg, Hauptstraße 7, 79104 Freiburg, Germany. claus-werner.franzke@uniklinik-freiburg.de.
Iris HelfrichSkin Cancer Unit of the Dermatology Department, Medical Faculty, West German Cancer Center, University Duisburg-Essen, 45147 Essen, Germany. iris.helfrich@uk-essen.de.
Deutschen Konsortium für Translationale Krebsforschung · DEUniversity Medical Center Freiburg · DEWest German Heart and Vascular Center Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Integrins represent a large family of cell receptors that mediate adhesion to the extracellular matrix (ECM), thereby modulating a variety of cellular functions that are required for proliferation, migration, malignant conversion and invasiveness. During tumorigenesis the conversion of a tumor cell from sessile, stationary phenotype to an invasive phenotype requires the ability of tumor cells to interact with their environment in order to transduce signals from the ECM into the cells. Hence, there is increasing evidence that changes in the composition, topography and tension of tumor matrix can be sensed by integrin receptors, leading to the regulation of intracellular signalling events which subsequently help to fuel cancer progression. The fact that intracellular signals perceived from integrin ligand binding impact on almost all steps of tumor progression, including tumor cell proliferation, survival, metastatic dissemination and colonization of a metastatic niche, renders integrins as ideal candidates for the development of therapeutic agents. In this review we summarize the role of integrins in cancer with the special focus on cancer therapies and the recent progress that has been made in the understanding of "integrin-induced tension in cancer". Finally, we conclude with clinical evidence for the role of integrin-mediated mechanotransduction in the development of therapy-resistant tumors.

Indexed as

AnimalsCell AdhesionCell Transformation, NeoplasticDrug Resistance, NeoplasmElasticityExtracellular MatrixHumansIntegrinsMechanotransduction, CellularNeoplasmsSignal TransductionTransforming Growth Factor betaIntegrinsTransforming Growth Factor betadrug-resistanceintegrinsmatrix stiffeningTGF-βtumor progression

Identifiers

PMID27854331
PMCPMC5133907
OpenAlexW2552455486

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.