Evidence map›Paper›PMID 27834816›Full record

ReviewCancers2016

Targeting the TAM Receptors in Leukemia.

Madeline G Huey, Katherine A Minson, H Shelton Earp, Deborah DeRyckere, Douglas K Graham

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Navigating TAM receptor dynamics in tumour immunotherapy.Cancer immunology, immunotherapy : CII · 2025
    Review
  5. Review
  6. Article
  7. Mertk: An emerging target in cancer biology and immuno-oncology.International review of cell and molecular biology · 2022
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Immune Evasion Mechanism and AXL.Frontiers in oncology · 2021
    Review
  13. AXL, an Important Host Factor for DENV and ZIKV Replication.Frontiers in cellular and infection microbiology · 2021
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Targeting Tyrosine Kinases in Acute Myeloid Leukemia: Why, Who and How?International journal of molecular sciences · 2019
    Review
  19. Review
  20. Article
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 2 institutions in 1 country.

Madeline G HueyAflac Cancer Center of Children's Healthcare of Atlanta, Department of Pediatrics, Emory University, Atlanta, GA 30322, USA. madeline.huey@emory.edu.
Katherine A MinsonAflac Cancer Center of Children's Healthcare of Atlanta, Department of Pediatrics, Emory University, Atlanta, GA 30322, USA. katherine.minson@emory.edu.
H Shelton EarpUNC Lineberger Comprehensive Cancer Center, Departments of Medicine and Pharmacology, University of North Carolina, Chapel Hill, NC 27514, USA. shelton_earp@med.unc.edu.
Deborah DeRyckereAflac Cancer Center of Children's Healthcare of Atlanta, Department of Pediatrics, Emory University, Atlanta, GA 30322, USA. deborah.deryckere@emory.edu.
Douglas K GrahamAflac Cancer Center of Children's Healthcare of Atlanta, Department of Pediatrics, Emory University, Atlanta, GA 30322, USA. douglas.graham@choa.org.
Emory University · USUniversity of North Carolina at Chapel Hill · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeted inhibition of members of the TAM (TYRO-3, AXL, MERTK) family of receptor tyrosine kinases has recently been investigated as a novel strategy for treatment of hematologic malignancies. The physiologic functions of the TAM receptors in innate immune control, natural killer (NK) cell differentiation, efferocytosis, clearance of apoptotic debris, and hemostasis have previously been described and more recent data implicate TAM kinases as important regulators of erythropoiesis and megakaryopoiesis. The TAM receptors are aberrantly or ectopically expressed in many hematologic malignancies including acute myeloid leukemia, B- and T-cell acute lymphoblastic leukemia, chronic lymphocytic leukemia, and multiple myeloma. TAM receptors contribute to leukemic phenotypes through activation of pro-survival signaling pathways and interplay with other oncogenic proteins such as FLT3, LYN, and FGFR3. The TAM receptors also contribute to resistance to both cytotoxic chemotherapeutics and targeted agents, making them attractive therapeutic targets. A number of translational strategies for TAM inhibition are in development, including small molecule inhibitors, ligand traps, and monoclonal antibodies. Emerging areas of research include modulation of TAM receptors to enhance anti-tumor immunity, potential roles for TYRO-3 in leukemogenesis, and the function of the bone marrow microenvironment in mediating resistance to TAM inhibition.

Indexed as

AXLGas6hematopoiesisleukemiaMERTKmultiple myelomaresistancesignaling pathwaysTYRO3tyrosine kinase inhibitor

Identifiers

PMID27834816
PMCPMC5126761
OpenAlexW2555309153

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.