Related Experiment Video
Updated: Oct 12, 2025

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
Published on: August 11, 2017
Targeting MERTK and AXL in EGFR Mutant Non-Small Cell Lung Cancer
Dan Yan1, H Shelton Earp2,3, Deborah DeRyckere1
1Aflac Cancer and Blood Disorders Center, Children's Healthcare of Atlanta, Department of Pediatrics, Emory University, Atlanta, GA 30322, USA.
Abstract:
MERTK and AXL are members of the TAM family of receptor tyrosine kinases and are abnormally expressed in 69% and 93% of non-small cell lung cancers (NSCLCs), respectively. Expression of MERTK and/or AXL provides a survival advantage for NSCLC cells and correlates with lymph node metastasis, drug resistance, and disease progression in patients with NSCLC. The TAM receptors on host tumor infiltrating cells also play important roles in the immunosuppressive tumor microenvironment. Thus, MERTK and AXL are attractive biologic targets for NSCLC treatment. Here, we will review physiologic and oncologic roles for MERTK and AXL with an emphasis on the potential to target these kinases in NSCLCs with activating EGFR mutations.
Insights
MERTK and AXL receptor tyrosine kinases are highly expressed in non-small cell lung cancer (NSCLC), promoting tumor growth and resistance. Targeting these TAM kinases offers a promising therapeutic strategy for NSCLC, especially with EGFR mutations.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- MERTK and AXL are TAM family receptor tyrosine kinases.
- Abnormal expression observed in 69% (MERTK) and 93% (AXL) of non-small cell lung cancers (NSCLCs).
- Expression linked to survival advantage, metastasis, drug resistance, and disease progression in NSCLC.
Purpose of the Study:
- Review the physiologic and oncologic roles of MERTK and AXL.
- Highlight the potential of targeting MERTK and AXL in NSCLC treatment.
- Focus on NSCLCs with activating EGFR mutations.
Main Methods:
- Literature review of MERTK and AXL functions in NSCLC.
- Analysis of TAM receptor roles in the tumor microenvironment.
- Exploration of therapeutic targeting strategies.
Main Results:
- MERTK and AXL expression significantly impacts NSCLC progression.
- TAM receptors contribute to an immunosuppressive tumor microenvironment.
- Targeting MERTK/AXL is a viable strategy for NSCLC therapy.
Conclusions:
- MERTK and AXL are critical oncogenic drivers in NSCLC.
- Targeting TAM kinases presents a therapeutic opportunity.
- EGFR-mutated NSCLCs may benefit from MERTK/AXL inhibition.
More Related Videos
08:52Profiling Sensitivity to Targeted Therapies in EGFR-Mutant NSCLC Patient-Derived Organoids
Published on: November 22, 2021
09:38Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib
Published on: June 26, 2019
Related Concept Videos
Mitogens and the Cell Cycle
Targeted Cancer Therapies
There are several types of targeted therapies against...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...