Evidence map›Paper›PMID 32417270›Full record

ReviewPharmacology & therapeutics2020

MERTK in cancer therapy: Targeting the receptor tyrosine kinase in tumor cells and the immune system.

Justus M Huelse, Diana M Fridlyand, Shelton Earp, Deborah DeRyckere, Douglas K Graham

Erratum issuedOpen access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.3field-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

58 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. 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
  8. Article
  9. Genetic variants ofFrontiers in immunology · 2026
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Recent advances in TAM mechanisms in lung diseases.Journal of translational medicine · 2025
    Review
  15. Review
  16. Navigating TAM receptor dynamics in tumour immunotherapy.Cancer immunology, immunotherapy : CII · 2025
    Review
  17. AXL signaling in cancer: from molecular insights to targeted therapies.Signal transduction and targeted therapy · 2025
    Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Justus M HuelseAflac Cancer and Blood Disorders Center, Children's Healthcare of Atlanta, Department of Pediatrics, Emory University, Atlanta, GA, USA.
Diana M FridlyandAflac Cancer and Blood Disorders Center, Children's Healthcare of Atlanta, Department of Pediatrics, Emory University, Atlanta, GA, USA.
Shelton EarpLineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.
Deborah DeRyckereAflac Cancer and Blood Disorders Center, Children's Healthcare of Atlanta, Department of Pediatrics, Emory University, Atlanta, GA, USA.
Douglas K GrahamAflac Cancer and Blood Disorders Center, Children's Healthcare of Atlanta, Department of Pediatrics, Emory University, Atlanta, GA, USA. Electronic address: Douglas.Graham@choa.org.
Emory University · USAflac (United States) · USUNC Lineberger Comprehensive Cancer Center

Funding

Project 3: Targeting Bax signaling to overcome treatment resistance in NSCLCP50CA217691 · NCI · EMORY UNIVERSITY · PI FU, HAIAN, RAMALINGAM, SURESH S · 2019 to 2024
$10.1M
Research Training in Pediatric Non-Malignant HematologyT32HL139443 · NHLBI · EMORY UNIVERSITY · PI Clinton H Joiner, Shannon L. Meeks · 2018 to 2026
$2.6M
NCI NIH HHS P50 CA217691NHLBI NIH HHS T32 HL139443
6 · The paper itself

Abstract

The receptor tyrosine kinase MERTK is aberrantly expressed in numerous human malignancies, and is a novel target in cancer therapeutics. Physiologic roles of MERTK include regulation of tissue homeostasis and repair, innate immune control, and platelet aggregation. However, aberrant expression in a wide range of liquid and solid malignancies promotes neoplasia via growth factor independence, cell cycle progression, proliferation and tumor growth, resistance to apoptosis, and promotion of tumor metastases. Additionally, MERTK signaling contributes to an immunosuppressive tumor microenvironment via induction of an anti-inflammatory cytokine profile and regulation of the PD-1 axis, as well as regulation of macrophage, myeloid-derived suppressor cell, natural killer cell and T cell functions. Various MERTK-directed therapies are in preclinical development, and clinical trials are underway. In this review we discuss MERTK inhibition as an emerging strategy for cancer therapy, focusing on MERTK expression and function in neoplasia and its role in mediating resistance to cytotoxic and targeted therapies as well as in suppressing anti-tumor immunity. Additionally, we review preclinical and clinical pharmacological strategies to target MERTK.

Indexed as

AnimalsAntineoplastic Agentsc-Mer Tyrosine KinaseDrug Resistance, NeoplasmHumansMolecular Targeted TherapyNeoplasmsProtein Kinase InhibitorsTumor MicroenvironmentAntineoplastic Agentsc-Mer Tyrosine KinaseMERTK protein, humanProtein Kinase Inhibitorsanti-tumor immunityclinical trialsMERTKneoplasiapreclinical agents

Identifiers

PMID32417270
PMCPMC9847360
OpenAlexW3025897576

What Socratic 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 Socratic graph.