Evidence map›Paper›PMID 9034607›Full record

ReviewCancer metastasis reviews1996

Role of intermediate filaments in migration, invasion and metastasis.

M J Hendrix, E A Seftor, Y W Chu, K T Trevor, R E Seftor

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cancer metastasis reviews, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 264 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. CK19 Predicts Recurrence and Prognosis of HBV Positive HCC.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2022
    Article
  6. Article
  7. Article
  8. Recent insight into intermediate filament structure.Current opinion in cell biology · 2021
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Cytokeratin 19International journal of molecular sciences · 2018
    Article
  17. Types I and II Keratin Intermediate Filaments.Cold Spring Harbor perspectives in biology · 2018
    Review
  18. Article
  19. Article
  20. Article

25 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

5 authors at 3 institutions in 2 countries.

M J HendrixDepartment of Anatomy, College of Medicine, University of Iowa, Iowa City 52242-1109, USA.
E A Seftor
Y W Chu
K T Trevor
R E Seftor
University of Iowa · USAurora St. Luke's Medical Center · USInstitute of Biomedical Sciences, Academia Sinica · TW

Funding

Endothelial Transdifferentiation of Invasive Tumor CellsR37CA059702 · NCI · UNIVERSITY OF IOWA · PI HENDRIX, MARY J.C. · 2002 to 2011
$3.9M
CYTOKERATIN AND VIMENTIN EXPRESSION UNDERLIES METASTASISR01CA059702 · NCI · UNIVERSITY OF IOWA · PI HENDRIX, MARY J.C. · 1993 to 2000
$244k
NCI NIH HHS CA59702
6 · The paper itself

Abstract

The expression of intermediate filament proteins is remarkably tissue-specific which suggests that the intermediate filament (IF) type(s) present in cells is somehow related to their biological function. However, in some cancers-particularly malignant melanoma and breast carcinoma, there is a strong indication that vimentin and keratin IFs are coexpressed, thus presenting as a dedifferentiated or interconverted (between epithelial and mesenchymal) phenotype. In this review, two in vitro models are presented which recapitulate the interconverted phenotype in human melanoma and breast carcinoma, and allow, for the first time, unique observations to be made with respect to the role of IFs in cancer progression. These studies have provided direct evidence linking overexpression of keratin IFs in human melanoma with increased migratory and invasive activity in vitro, which can be down-regulated by substituting dominant-negative keratin mutants. Overexpression of vimentin IFs in the breast carcinoma model leads to augmentation of motility and invasiveness in vitro, which can be transiently down-regulated by treatment with antisense oligonucleotides to vimentin. Additional experimental evidence suggests that the mechanism(s) responsible for the differential expression of metastatic properties associated with the interconverted phenotype rest(s) in the unique interaction, either direct or indirect, of IFs with specific integrins interacting with the extracellular matrix. In this review, we discuss the observations derived from the human melanoma and breast carcinoma models to address the hypothesis that the ability to coexpress vimentin and keratins confers a selective advantage to tumor cells in their interpretation of and response to signaling cues from the extracellular matrix. The ramifications of these observations are discussed with respect to the patholophysiology of the respective in situ tumors.

Indexed as

AnimalsBreast NeoplasmsCell MovementHumansIntermediate Filament ProteinsIntermediate FilamentsMelanomaNeoplasm InvasivenessNeoplasm MetastasisIntermediate Filament Proteins

Identifiers

PMID9034607
OpenAlexW2094543320

What OpenQuestion holds

Textmetadata
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.