Evidence map›Paper›PMID 21196205›Full record

ReviewFrontiers in bioscience (Landmark edition)2011

Epithelial and mesenchymal phenotypic switchings modulate cell motility in metastasis.

Alan Wells, Yvonne L Chao, Jelena Grahovac, Qian Wu, Douglas A Lauffenburger

Open access · bronzeAbstract readReview
In one paragraph

Review in Frontiers in bioscience (Landmark edition), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Effects of heavy ions (Translational cancer research · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. A Perspective on Therapeutic Pan-Resistance in Metastatic Cancer.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Review
  17. Article
  18. Study on the Drug Targets and Molecular Mechanisms ofEvidence-based complementary and alternative medicine : eCAM · 2020
    Article
  19. Article
  20. Article
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

5 authors at 1 institution in 1 country.

Alan WellsDepartment of Pathology, Pittsburgh VAMC and University of Pittsburgh, Pittsburgh, PA 15213, USA. wellsa@upmc.edu
Yvonne L Chao
Jelena Grahovac
Qian Wu
Douglas A Lauffenburger
UPMC Health System · US

Funding

Spatial Segregation of Cell Functioning During MotilityR01GM069668 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WELLS, ALAN · 2004 to 2019
$4.7M
Bioengineering Polymers for Parsing Cell ResponsesR01DE019523 · NIDCR · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GRIFFITH, LINDA G · 2008 to 2012
$1.7M
Computational Modeling of Cell Migration in 3D MatricesR01GM081336 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2008 to 2011
$1.1M
Cell Motility in Prostate Tumor InvasionR01CA088865 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2001 to 2004
$991k
Molecular Regulation of Cancer ProgressionI01BX001017 · VA · VETERANS HEALTH ADMINISTRATION · PI WELLS, ALAN · 2012 to 2015
–
BLRD VA I01 BX001017NCI NIH HHS R01 CA088865NIDCR NIH HHS R01 DE019523NIGMS NIH HHS R01 GM069668NIGMS NIH HHS R01 GM081336
6 · The paper itself

Abstract

The most ominous stage of cancer progression is metastasis, or the dissemination of carcinoma cells from the primary site into distant organs. Metastases are often resistant to current extirpative therapies and even the newest biological agents cure only a small subset of patients. Therefore a greater understanding of tumor biology that integrates properties intrinsic to carcinomas with tissue environmental modulators of behavior is needed. In no aspect of tumor progression is this more evident than the acquisition of cell motility that is critical for both escape from the primary tumor and colonization. In this overview, we discuss how this behavior is modified by carcinoma cell phenotypic plasticity that is evidenced by reversible switching between epithelial and mesenchymal phenotypes. The presence or absence of intercellular adhesions mediate these switches and dictate the receptivity towards signals from the extracellular milieu. These signals, which include soluble growth factors, cytokines, and extracellular matrix embedded with matrikines and matricryptines will be discussed in depth. Finally, we will describe a new mode of discerning the balance between epithelioid and mesenchymal movement.

Indexed as

Epithelial-Mesenchymal TransitionCadherinsCell AdhesionCell MovementCell Transformation, NeoplasticCytokinesDesmosomesEpidermal Growth FactorExtracellular Matrix ProteinsGap JunctionsHepatocyte Growth FactorHumansInsulin-Like Growth Factor IIntegrinsNeoplasm MetastasisNeoplasmsCadherinsCytokinesEpidermal Growth FactorExtracellular Matrix ProteinsHepatocyte Growth FactorInsulin-Like Growth Factor IIntegrinsTransforming Growth Factor betaTumor Necrosis Factor-alpha

Identifiers

PMID21196205
PMCPMC4003907
OpenAlexW2001173684

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.