Evidence map›Paper›PMID 28258690›Full record

ReviewImmunological reviews2017

TAM receptor tyrosine kinases as emerging targets of innate immune checkpoint blockade for cancer therapy.

Yemsratch T Akalu, Carla V Rothlin, Sourav Ghosh

Abstract readReview
In one paragraph

Review in Immunological reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

100 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  4. MRTX-500 Phase 2 Trial: Sitravatinib With Nivolumab in Patients With Nonsquamous NSCLC Progressing On or After Checkpoint Inhibitor Therapy or Chemotherapy.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2023
    Trial
  5. Randomized Phase II Trial and Tumor Mutational Spectrum Analysis from Cabozantinib versus Chemotherapy in Metastatic Uveal Melanoma (Alliance A091201).Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    Trial
  6. Article
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  9. Review
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  14. Current Perspectives of Immunotherapy for Hepatocellular Carcinoma.Combinatorial chemistry & high throughput screening · 2025
    Review
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  17. Small-molecule-based targeted therapy in liver cancer.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Review
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  19. Article
  20. Review

40 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

3 authors.

Yemsratch T AkaluDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.
Carla V RothlinDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.
Sourav GhoshDepartment of Pharmacology, Yale University School of Medicine, New Haven, CT, USA.

Funding

TAM receptor tyrosine kinases in inflammatory boweldiseaseR01AI089824 · NIAID · YALE UNIVERSITY · PI ROTHLIN, CARLA · 2010 to 2018
$3.9M
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI089824
6 · The paper itself

Abstract

Cancer immunotherapy utilizing T-cell checkpoint inhibitors has shown tremendous clinical success. Yet, this mode of treatment is effective in only a subset of patients. Unresponsive patients tend to have non-T-cell-inflamed tumors that lack markers associated with the activation of adaptive anti-tumor immune responses. Notably, elimination of cancer cells by T cells is critically dependent on the optimal activity of innate immune cells. Therefore, identifying new targets that regulate innate immune cell function and promote the engagement of adaptive tumoricidal responses is likely to lead to the development of improved therapies against cancer. Here, we review the TAM receptor tyrosine kinases-TYRO3, AXL, and MERTK-as an emerging class of innate immune checkpoints that participate in key steps of anti-tumoral immunity. Namely, TAM-mediated efferocytosis, negative regulation of dendritic cell activity, and dysregulated production of chemokines collectively favor the escape of malignant cells. Hence, disabling TAM signaling may promote engagement of adaptive immunity and complement T-cell checkpoint blockade.

Indexed as

Immunity, InnateAdaptive ImmunityAnimalsAntibodies, MonoclonalAxl Receptor Tyrosine Kinasec-Mer Tyrosine KinaseCostimulatory and Inhibitory T-Cell ReceptorsDrug Therapy, CombinationHumansImmunotherapyNeoplasmsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesSignal TransductionTumor EscapeAntibodies, MonoclonalAXL protein, humanAxl Receptor Tyrosine Kinasec-Mer Tyrosine KinaseCostimulatory and Inhibitory T-Cell ReceptorsMERTK protein, humanProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesTYRO3 protein, humanAXLinnate immune checkpointsMERTKTYRO3

Identifiers

PMID28258690
PMCPMC5381815

What OpenQuestion holds

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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.