Evidence map›Paper›PMID 27014069›Full record

ReviewFrontiers in pharmacology2016

Discoidin Domain Receptors: Potential Actors and Targets in Cancer.

Hassan Rammal, Charles Saby, Kevin Magnien, Laurence Van-Gulick, Roselyne Garnotel, Emilie Buache, Hassan El Btaouri, Pierre Jeannesson, Hamid Morjani

RetractedErratum issuedOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
9.9field-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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Discoid Domain Receptors Signaling in Macrophages-Mediated Diseases.International journal of general medicine · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
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  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
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14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Hassan RammalExtracellular Matrix and Cellular Dynamics, Faculty of Pharmacy, MEDyC Centre National de la Recherche Scientifique UMR7369 Reims, France.
Charles SabyExtracellular Matrix and Cellular Dynamics, Faculty of Pharmacy, MEDyC Centre National de la Recherche Scientifique UMR7369 Reims, France.
Kevin MagnienExtracellular Matrix and Cellular Dynamics, Faculty of Pharmacy, MEDyC Centre National de la Recherche Scientifique UMR7369 Reims, France.
Laurence Van-GulickExtracellular Matrix and Cellular Dynamics, Faculty of Pharmacy, MEDyC Centre National de la Recherche Scientifique UMR7369 Reims, France.
Roselyne GarnotelExtracellular Matrix and Cellular Dynamics, Faculty of Pharmacy, MEDyC Centre National de la Recherche Scientifique UMR7369 Reims, France.
Emilie BuacheExtracellular Matrix and Cellular Dynamics, Faculty of Pharmacy, MEDyC Centre National de la Recherche Scientifique UMR7369 Reims, France.
Hassan El BtaouriExtracellular Matrix and Cellular Dynamics, Faculty of Pharmacy, MEDyC Centre National de la Recherche Scientifique UMR7369 Reims, France.
Pierre JeannessonExtracellular Matrix and Cellular Dynamics, Faculty of Pharmacy, MEDyC Centre National de la Recherche Scientifique UMR7369 Reims, France.
Hamid MorjaniExtracellular Matrix and Cellular Dynamics, Faculty of Pharmacy, MEDyC Centre National de la Recherche Scientifique UMR7369 Reims, France.
Biologie cellulaire et Cancer · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The extracellular matrix critically controls cancer cell behavior by inducing several signaling pathways through cell membrane receptors. Besides conferring structural properties to tissues around the tumor, the extracellular matrix is able to regulate cell proliferation, survival, migration, and invasion. Among these receptors, the integrins family constitutes a major class of receptors that mediate cell interactions with extracellular matrix components. Twenty years ago, a new class of extracellular matrix receptors has been discovered. These tyrosine kinase receptors are the two discoidin domain receptors DDR1 and DDR2. DDR1 was first identified in the Dictyostelium discoideum and was shown to mediate cell aggregation. DDR2 shares highly conserved sequences with DDR1. Both receptors are activated upon binding to collagen, one of the most abundant proteins in extracellular matrix. While DDR2 can only be activated by fibrillar collagen, particularly types I and III, DDR1 is mostly activated by type I and IV collagens. In contrast with classical growth factor tyrosine kinase receptors which display a rapid and transient activation, DDR1 and DDR2 are unique in that they exhibit delayed and sustained receptor phosphorylation upon binding to collagen. Recent studies have reported differential expression and mutations of DDR1 and DDR2 in several cancer types and indicate clearly that these receptors have to be taken into account as new players in the different aspects of tumor progression, from non-malignant to highly malignant and invasive stages. This review will discuss the current knowledge on the role of DDR1 and DDR2 in malignant transformation, cell proliferation, epithelial to mesenchymal transition, migratory, and invasive processes, and finally the modulation of the response to chemotherapy. These new insights suggest that DDR1 and DDR2 are new potential targets in cancer therapy.

Indexed as

cancercell signalingcollagendiscoidin domain receptorsextracellular matrixtargeted therapytyrosine kinase

Identifiers

PMID27014069
PMCPMC4789497
OpenAlexW2304570313

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.