Evidence map›Paper›PMID 22366781›Full record

ReviewCancer metastasis reviews2012

Discoidin domain receptor tyrosine kinases: new players in cancer progression.

Rajeshwari R Valiathan, Marta Marco, Birgit Leitinger, Celina G Kleer, Rafael Fridman

Abstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2012. 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
14.1field-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, 374 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Overexpression ofJournal of biomedical research · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Discoid Domain Receptors Signaling in Macrophages-Mediated Diseases.International journal of general medicine · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024
    Review
  20. Article

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

5 authors at 3 institutions in 2 countries.

Rajeshwari R ValiathanDepartment of Pathology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Marta Marco
Birgit Leitinger
Celina G Kleer
Rafael Fridman
Wayne State University · USImperial College London · GBUniversity of Michigan–Ann Arbor · US

Funding

Role of EZH2 in Breast Cancer ProgressionR01CA107469 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Celina G Kleer · 2005 to 2026
$5.9M
Role of CCN6 (WISP3) in the Progression and Metastasis of Breast Cancer.R01CA125577 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Celina G Kleer · 2008 to 2026
$5.5M
REGULATION OF MATRIX METALLOPROTEINASE ACTIVATIONR01CA061986 · NCI · WAYNE STATE UNIVERSITY · PI FRIDMAN, RAFAEL A. · 1995 to 2015
$3.9M
Biotechnology and Biological Sciences Research Council BB/IO11226/1Medical Research Council G0701121NCI NIH HHS CA-107469NCI NIH HHS R01 CA061986NCI NIH HHS R01 CA107469NCI NIH HHS R01 CA-125577NCI NIH HHS R01 CA125577NCI NIH HHS R01 CA-61986
6 · The paper itself

Abstract

Almost all human cancers display dysregulated expression and/or function of one or more receptor tyrosine kinases (RTKs). The strong causative association between altered RTK function and cancer progression has been translated into novel therapeutic strategies that target these cell surface receptors in cancer. Yet, the full spectrum of RTKs that may alter the oncogenic process is not completely understood. Accumulating evidence suggests that a unique set of RTKs known as the discoidin domain receptors (DDRs) play a key role in cancer progression by regulating the interactions of tumor cells with their surrounding collagen matrix. The DDRs are the only RTKs that specifically bind to and are activated by collagen. DDRs control cell and tissue homeostasis by acting as collagen sensors, transducing signals that regulate cell polarity, tissue morphogenesis, and cell differentiation. In cancer, DDRs are hijacked by tumor cells to disrupt normal cell-matrix communication and initiate pro-migratory and pro-invasive programs. Importantly, several cancer types exhibit DDR mutations, which are thought to alter receptor function and contribute to cancer progression. Other evidence suggests that the actions of DDRs in cancer are complex, either promoting or suppressing tumor cell behavior in a DDR type/isoform specific- and context-dependent manner. Thus, there is still a considerable gap in our knowledge of DDR actions in cancer tissues. This review summarizes and discusses the current knowledge on DDR expression and function in cancer. It is hoped that this effort will encourage more research into these poorly understood but unique RTKs, which have the potential of becoming novel therapeutic targets in cancer.

Indexed as

AnimalsCollagenDiscoidin Domain ReceptorsDisease ProgressionEnzyme ActivationGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyMutationNeoplasmsProtein BindingProtein Processing, Post-TranslationalProtein Structure, TertiaryReceptor Protein-Tyrosine KinasesReceptors, MitogenSignal TransductionCollagenDiscoidin Domain ReceptorsReceptor Protein-Tyrosine KinasesReceptors, Mitogen

Identifiers

PMID22366781
PMCPMC3351584
OpenAlexW2145449209

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.