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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
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Related Experiment Video

Updated: Oct 23, 2025

Author Spotlight: Establishing a Murine Non-Small Cell Lung Cancer Model for Developing Nanoformulations of Anticancer Drugs
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Targeting AXL in NSCLC.

Aubhishek Zaman1,2, Trever G Bivona1,2

  • 1Department of Medicine, University of California, San Francisco, CA, USA.

Lung Cancer (Auckland, N.Z.)
|August 19, 2021
PubMed
Summary
This summary is machine-generated.

AXL receptor tyrosine kinase drives resistance to cancer therapies, particularly in non-small-cell lung cancer (NSCLC). Targeting AXL offers a promising strategy to overcome drug resistance and improve precision medicine outcomes.

Keywords:
AXLdrug resistancelung cancertargeted therapy

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Precision medicine in cancer targets specific vulnerabilities, but therapy resistance limits efficacy.
  • AXL receptor tyrosine kinase is implicated in resistance across various cancers, including non-small-cell lung cancer (NSCLC).

Purpose of the Study:

  • To review AXL biology in normal homeostasis, oncogenesis, and therapy resistance, with a focus on NSCLC.
  • To delineate AXL's role in resistance to targeted therapies (e.g., EGFR inhibitors) and chemotherapy in NSCLC.
  • To explore AXL's contribution to resistance mechanisms like epithelial-mesenchymal transition (EMT), tumor microenvironment, and heterogeneity.

Main Methods:

  • Literature review of AXL biology and its role in NSCLC therapy resistance.
  • Analysis of AXL's involvement in key cellular processes modulating treatment response.
  • Cataloging and discussion of emerging pharmacologic agents targeting AXL.

Main Results:

  • AXL mediates resistance to tyrosine kinase inhibitors (TKIs) and chemotherapy in NSCLC.
  • AXL influences EMT, tumor microenvironment, and heterogeneity, contributing to drug resistance.
  • Several pharmacologic strategies are emerging to target AXL-mediated resistance.

Conclusions:

  • Understanding AXL biology is crucial for predicting and enhancing targeted therapies in NSCLC.
  • Targeting AXL, potentially through combination therapies, may overcome drug resistance and improve outcomes across diverse NSCLC subtypes.
  • Further research into AXL-targeted precision medicine is needed to address challenges and optimize treatment strategies.