Evidence map›Paper›PMID 23833304›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2013

Molecular pathways: MERTK signaling in cancer.

Christopher T Cummings, Deborah Deryckere, H Shelton Earp, Douglas K Graham

Open access · greenAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
4.4field-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

89 citing papers in PubMed, 143 citations in OpenAlex.

  1. Article
  2. Article
  3. A systems approach identifies MERTK as a therapeutic vulnerability in ZFTA-RELA-driven ependymomas.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Review
  5. Genetic variants ofFrontiers in immunology · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Recent advances in TAM mechanisms in lung diseases.Journal of translational medicine · 2025
    Review
  14. Review
  15. Navigating TAM receptor dynamics in tumour immunotherapy.Cancer immunology, immunotherapy : CII · 2025
    Review
  16. Article
  17. Article
  18. Review
  19. The Evolving Applications of Bispecific Antibodies: Reaping the Harvest of Early Sowing and Planting New Seeds.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025
    Review
  20. Article

29 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

4 authors at 2 institutions in 1 country.

Christopher T CummingsAuthors' Affiliations: Department of Pediatrics, Section of Hematology, Oncology and Bone Marrow Transplantation, University of Colorado Anschutz Medical Campus, Aurora, Colorado; and Departments of Medicine and Pharmacology, UNC Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Deborah Deryckere
H Shelton Earp
Douglas K Graham
University of Colorado Anschutz Medical Campus · USUniversity of North Carolina at Chapel Hill · US

Funding

Novel Biologically Targeted Therapy Against the Mer and Axl Receptor Tyrosine KinR01CA137078 · NCI · UNIVERSITY OF COLORADO DENVER · PI GRAHAM, DOUGLAS K · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA137078NCI NIH HHS R01CA137078
6 · The paper itself

Abstract

MERTK is a receptor tyrosine kinase of the TAM (Tyro3, Axl, MERTK) family, with a defined spectrum of normal expression. However, MERTK is overexpressed or ectopically expressed in a wide variety of cancers, including leukemia, non-small cell lung cancer, glioblastoma, melanoma, prostate cancer, breast cancer, colon cancer, gastric cancer, pituitary adenomas, and rhabdomyosarcomas, potentially resulting in the activation of several canonical oncogenic signaling pathways. These include the mitogen-activated protein kinase and phosphoinositide 3-kinase pathways, as well as regulation of signal transducer and activator of transcription family members, migration-associated proteins including the focal adhesion kinase and myosin light chain 2, and prosurvival proteins such as survivin and Bcl-2. Each has been implicated in MERTK physiologic and oncogenic functions. In neoplastic cells, these signaling events result in functional phenotypes such as decreased apoptosis, increased migration, chemoresistance, increased colony formation, and increased tumor formation in murine models. Conversely, MERTK inhibition by genetic or pharmacologic means can reverse these pro-oncogenic phenotypes. Multiple therapeutic approaches to MERTK inhibition are currently in development, including ligand "traps", a monoclonal antibody, and small-molecule tyrosine kinase inhibitors.

Indexed as

Signal TransductionAntineoplastic Agentsc-Mer Tyrosine KinaseHumansNeoplasmsProtein Kinase InhibitorsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesTranslational Research, BiomedicalAntineoplastic Agentsc-Mer Tyrosine KinaseMERTK protein, humanProtein Kinase InhibitorsProto-Oncogene ProteinsReceptor Protein-Tyrosine Kinases

Identifiers

PMID23833304
PMCPMC10039640
OpenAlexW2132169351

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.