Evidence map›Paper›PMID 21362138›Full record

ReviewThe FEBS journal2011

Hyaluronan-CD44 interactions as potential targets for cancer therapy.

Suniti Misra, Paraskevi Heldin, Vincent C Hascall, Nikos K Karamanos, Spyros S Skandalis, Roger R Markwald, Shibnath Ghatak

Open access · bronzeAbstract readReview
In one paragraph

Review in The FEBS journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers.

0numbers the graph read from it
0cells of the map it votes in
203citing papers in PubMed
13.4field-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

203 citing papers in PubMed, 473 citations in OpenAlex.

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  19. Glycosylation in Cancer.Handbook of experimental pharmacology · 2025
    Review
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143 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

7 authors at 5 institutions in 4 countries.

Suniti MisraRegenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC 29425, USA. misra@musc.edu
Paraskevi Heldin
Vincent C Hascall
Nikos K Karamanos
Spyros S Skandalis
Roger R Markwald
Shibnath Ghatak
Medical University of South Carolina · USCleveland Clinic · USLudwig Cancer Research · SELudwig Cancer Research · BEUniversity of Patras · GR

Funding

UBIQUITIN CARBOXYL TERMINAL HYDROLASE L1 (UCH-L1) AND VASCULAR LESION FORMATIONP20RR016434 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MARKWALD, ROGER R · 2001 to 2011
$24.8M
UNDERSTANDING AND CONTROLLING TISSUE-SPECIFIC VASCULAR PATTERNINGP20RR021949 · NCRR · CLEMSON UNIVERSITY · PI MARKWALD, ROGER R · 2009 to 2011
$5.2M
MUCOPOLYSACCHRIDE METABOLISM IN CARDIAC ANOMALIESR01HL033756 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MARKWALD, ROGER R · 1985 to 2015
$4.8M
Robotics CoreP30AR050953 · NIAMS · CLEVELAND CLINIC LERNER COM-CWRU · PI HASCALL, VINCENT CHARLES · 2004 to 2008
$2.9M
NCRR NIH HHS P20 RR016434NCRR NIH HHS P20RR016434NCRR NIH HHS P20 RR021949NCRR NIH HHS P20RR021949NHLBI NIH HHS HL R01 33756NHLBI NIH HHS R01 HL033756NIAMS NIH HHS 1 P30AR050953NIAMS NIH HHS P30 AR050953
6 · The paper itself

Abstract

It is becoming increasingly clear that signals generated in tumor microenvironments are crucial to tumor cell behavior, such as survival, progression and metastasis. The establishment of these malignant behaviors requires that tumor cells acquire novel adhesion and migration properties to detach from their original sites and to localize to distant organs. CD44, an adhesion/homing molecule, is a major receptor for the glycosaminoglycan hyaluronan, which is one of the major components of the tumor extracellular matrix. CD44, a multistructural and multifunctional molecule, detects changes in extracellular matrix components, and thus is well positioned to provide appropriate responses to changes in the microenvironment, i.e. engagement in cell-cell and cell-extracellular matrix interactions, cell trafficking, lymph node homing and the presentation of growth factors/cytokines/chemokines to co-ordinate signaling events that enable the cell responses that change in the tissue environment. The potential involvement of CD44 variants (CD44v), especially CD44v4-v7 and CD44v6-v9, in tumor progression has been confirmed for many tumor types in numerous clinical studies. The downregulation of the standard CD44 isoform (CD44s) in colon cancer is postulated to result in increased tumorigenicity. CD44v-specific functions could be caused by their higher binding affinity than CD44s for hyaluronan. Alternatively, CD44v-specific functions could be caused by differences in associating molecules, which may bind selectively to the CD44v exon. This minireview summarizes how the interaction between hyaluronan and CD44v can serve as a potential target for cancer therapy, in particular how silencing CD44v can target multiple metastatic tumors.

Indexed as

HumansHyaluronan ReceptorsHyaluronic AcidNeoplasm MetastasisNeoplasmsSignal TransductionHyaluronan ReceptorsHyaluronic Acid

Identifiers

PMID21362138
PMCPMC3166356
OpenAlexW1873369382

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.