Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Immune cell landscape reveals 5 immune-related subtypes and molecular characteristics with prognostic and therapeutic implications in pan-cancer.

Journal of leukocyte biology·2026
Same author

An Integrative Strategy Delineates Modular Metabolic Remodeling and Potential Therapeutic Targets Across Metabolic Diseases.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Deciphering the Transcription Factor-Dominated Ecosystem During Esophageal Squamous Cell Carcinoma Progression at the Single-Cell Level.

International journal of molecular sciences·2026
Same author

Uncovering the Key Circuit FOSL2/FOS/EGR3/EGR1, Contributing to the Hyperexcitability of Excitatory Neurons in the Epileptic Temporal Cortex and Hippocampus.

International journal of molecular sciences·2026
Same author

Integrating Multi-Omics Atlas to Uncover Genetic and Epigenetic Mechanisms and Reveal Cell State Evolution Across Ecotypes in Male Urological Cancers.

International journal of molecular sciences·2026
Same author

Dissecting glioblastoma risk signatures in the tumor immune microenvironment based on multi-dimensional transcriptomics.

GigaScience·2026

Related Experiment Video

Updated: May 14, 2026

Profiling Sensitivity to Targeted Therapies in EGFR-Mutant NSCLC Patient-Derived Organoids
08:52

Profiling Sensitivity to Targeted Therapies in EGFR-Mutant NSCLC Patient-Derived Organoids

Published on: November 22, 2021

Coordinated Multicellular Immune Programs and Drug Targets Revealed by Single-Cell Analysis in Driver-Mutated NSCLC.

Kuan Yang1, Kaiyue Yang1, Jiasi Wang1

  • 1College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China.

International Journal of Molecular Sciences
|May 13, 2026
PubMed
Summary

Oncogenic driver mutations in non-small cell lung cancer create distinct tumor immune microenvironment (TIME) architectures. These multicellular modules impact patient outcomes and offer targets for precision immunotherapy.

Keywords:
driver mutatedimmune coordinationmalignant regulatory networkprognostic biomarkerssingle-cell transcriptomics

More Related Videos

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

Related Experiment Videos

Last Updated: May 14, 2026

Profiling Sensitivity to Targeted Therapies in EGFR-Mutant NSCLC Patient-Derived Organoids
08:52

Profiling Sensitivity to Targeted Therapies in EGFR-Mutant NSCLC Patient-Derived Organoids

Published on: November 22, 2021

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

Area of Science:

  • Oncology
  • Immunology
  • Genomics

Background:

  • Oncogenic driver mutations in non-small cell lung cancer (NSCLC) shape tumor growth and the immune microenvironment.
  • The precise contribution of diverse cell interactions within the tumor immune microenvironment (TIME) to NSCLC progression is not fully understood.

Purpose of the Study:

  • To investigate the multicellular architecture of the TIME in relation to specific oncogenic driver mutations in NSCLC.
  • To identify distinct multicellular modules and their association with clinical outcomes and therapeutic vulnerabilities.

Main Methods:

  • Single-cell profiling of approximately 200,000 cells from 45 treatment-naïve NSCLC patients with seven major driver mutations.
  • Identification and characterization of five multicellular modules (CM1-5) based on cell-cell interactions and functional properties.
  • Development and validation of a driver mutation-specific prognostic signature (DMSP.sig) model.

Main Results:

  • Five distinct multicellular modules (CM1-5) were identified, each linked to specific malignant regulatory programs.
  • CM2 (associated with EGFR/MET mutations) showed invasive features in brain metastases, driven by astrocyte-myofibroblast crosstalk.
  • CM5 (enriched in ROS1/KRAS/EGFR mutations) exhibited immunosuppressive and pro-angiogenic signaling, promoting immune escape and vascular remodeling.
  • The DMSP.sig model effectively stratified patient survival and identified potential therapeutic targets.

Conclusions:

  • Oncogenic drivers sculpt unique TIME architectures in NSCLC.
  • Specific multicellular modules are associated with distinct clinical behaviors, such as brain metastasis and immune evasion.
  • The findings provide a framework for prognostic assessment and the development of precision immunotherapies for NSCLC.