Related Experiment Video

Updated: Sep 22, 2025

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

18.1K

Resistance to immune checkpoint inhibitors in KRAS-mutant non-small cell lung cancer

Yunchang Li1,2, Lanlin Hu1,2, Xinhao Peng1

  • 1Integrative Cancer Center and Cancer Clinical Research Center, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu 610042, Sichuan, China.

Cancer Drug Resistance (Alhambra, Calif.)
|May 18, 2022
PubMed

Insights

KRAS-mutant non-small cell lung cancer (NSCLC) shows varied responses to immunotherapy. This review explores resistance mechanisms and highlights metabolic pathways as potential strategies to improve treatment outcomes for NSCLC patients.

Area of Science:

  • Oncology
  • Immunotherapy
  • Cancer Metabolism

Background:

  • Non-small cell lung cancer (NSCLC) with KRAS mutations presents clinical heterogeneity and poor prognosis with standard therapies.
  • Immune checkpoint inhibitors (ICIs) have transformed NSCLC treatment, yet some KRAS-mutant NSCLC patients exhibit resistance.
  • Understanding resistance mechanisms is crucial for optimizing immunotherapy in KRAS-mutant NSCLC.

Purpose of the Study:

  • To elucidate mechanisms of immunotherapy resistance in KRAS-driven NSCLC.
  • To highlight the role of the tumor microenvironment (TME) in immunotherapy response.
  • To identify potential therapeutic strategies targeting cancer metabolism to overcome resistance.

Main Methods:

  • Literature review focusing on KRAS mutations in NSCLC and immunotherapy response.
  • Analysis of studies investigating tumor microenvironment alterations.
  • Exploration of cancer metabolism pathways in the context of immunotherapy resistance.

Main Results:

  • KRAS mutations influence TME composition and function, impacting ICI efficacy.
  • Immunoinhibitors and immunostimulators modulate the TME in KRAS-mutant NSCLC.
  • Aberrant cancer metabolism pathways contribute to immunotherapy resistance.

Conclusions:

  • Targeting specific metabolic pathways in the TME may overcome immunotherapy resistance in KRAS-mutant NSCLC.
  • Further research into TME modulation and metabolic reprogramming is warranted.
  • Personalized therapeutic strategies integrating immunotherapy with metabolic interventions show promise for improved patient outcomes.
Keywords:
KRAS mutationNon-small cell lung cancercancer metabolism.immune checkpoints inhibitorstumor microenvironments

More Related Videos

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure09:38

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

8.9K
Patient-Derived Tumor Explants As a "Live" Preclinical Platform for Predicting Drug Resistance in Patients07:42

Patient-Derived Tumor Explants As a "Live" Preclinical Platform for Predicting Drug Resistance in Patients

Published on: February 7, 2021

5.1K

Related Concept Videos

Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.4K
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
6.5K