Evidence map›Paper›PMID 28072762›Full record

ReviewBritish journal of cancer2017

Giving AXL the axe: targeting AXL in human malignancy.

Carl M Gay, Kavitha Balaji, Lauren Averett Byers

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 204 papers.

0numbers the graph read from it
0cells of the map it votes in
204citing papers in PubMed
11.8field-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

204 citing papers in PubMed, 337 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. AXL Inhibitors in Oncology Clinical Trials: A Review.Journal of immunotherapy and precision oncology · 2026
    Review
  13. [Role of Receptor Tyrosine Kinase AXL in Cancer Targeted Therapy Drug Resistance].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. ZDHHC11-mediated AXL palmitoylation promotes osimertinib resistance in non-small-cell lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  19. Review
  20. Article

144 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 at 1 institution in 1 country.

Carl M GayDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA.
Kavitha BalajiDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA.
Lauren Averett ByersDepartment of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
Therapeutic strategies for targeting PARP1 in small cell lung cancerR01CA207295 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Lauren Averett Byers · 2016 to 2026
$3.7M
NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA070907NCI NIH HHS R01 CA207295
6 · The paper itself

Abstract

The receptor tyrosine kinase AXL, activated by a complex interaction between its ligand growth arrest-specific protein 6 and phosphatidylserine, regulates various vital cellular processes, including proliferation, survival, motility, and immunologic response. Although not implicated as an oncogenic driver itself, AXL, a member of the TYRO3, AXL, and MERTK family of receptor tyrosine kinases, is overexpressed in several haematologic and solid malignancies, including acute myeloid leukaemia, non-small cell lung cancer, gastric and colorectal adenocarcinomas, and breast and prostate cancers. In the context of malignancy, evidence suggests that AXL overexpression drives wide-ranging processes, including epithelial to mesenchymal transition, tumour angiogenesis, resistance to chemotherapeutic and targeted agents, and decreased antitumor immune response. As a result, AXL is an attractive candidate not only as a prognostic biomarker in malignancy but also as a target for anticancer therapies. Several AXL inhibitors are currently in preclinical and clinical development. This article reviews the structure, regulation, and function of AXL; the role of AXL in the tumour microenvironment; the development of AXL as a therapeutic target; and areas of ongoing and future investigation.

Indexed as

AnimalsAxl Receptor Tyrosine KinaseCell ProliferationDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyNeoplasmsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesTumor MicroenvironmentAXL protein, humanAxl Receptor Tyrosine KinaseProto-Oncogene ProteinsReceptor Protein-Tyrosine Kinases

Identifiers

PMID28072762
PMCPMC5318970
OpenAlexW2568917916

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.