Related Experiment Video
Updated: May 10, 2026

Ultra-Fast Amplicon-Based Next-Generation Sequencing in Non-Squamous Non-Small Cell Lung Cancer
Published on: September 8, 2023
Molecularly targeted approaches herald a new era of non-small-cell lung cancer treatment
Hiroyasu Kaneda1, Takeshi Yoshida, Isamu Okamoto
1Department of Medical Oncology, Kinki University, Osakasayama, Japan.
Abstract:
The discovery of activating mutations in the epidermal growth-factor receptor (EGFR) gene in 2004 opened a new era of personalized treatment for non-small-cell lung cancer (NSCLC). EGFR mutations are associated with a high sensitivity to EGFR tyrosine kinase inhibitors, such as gefitinib and erlotinib. Treatment with these agents in EGFR-mutant NSCLC patients results in dramatically high response rates and prolonged progression-free survival compared with conventional standard chemotherapy. Subsequently, echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK), a novel driver oncogene, has been found in 2007. Crizotinib, the first clinically available ALK tyrosine kinase inhibitor, appeared more effective compared with standard chemotherapy in NSCLC patients harboring EML4-ALK. The identification of EGFR mutations and ALK rearrangement in NSCLC has further accelerated the shift to personalized treatment based on the appropriate patient selection according to detailed molecular genetic characterization. This review summarizes these genetic biomarker-based approaches to NSCLC, which allow the instigation of individualized therapy to provide the desired clinical outcome.
Insights
Personalized medicine for non-small-cell lung cancer (NSCLC) advanced with the discovery of EGFR and ALK mutations. Targeted therapies like gefitinib, erlotinib, and crizotinib offer improved outcomes for NSCLC patients with these specific genetic biomarkers.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Activating mutations in the epidermal growth-factor receptor (EGFR) gene were discovered in 2004.
- The echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion oncogene was identified in 2007.
- These discoveries marked a shift towards personalized treatment in non-small-cell lung cancer (NSCLC).
Purpose of the Study:
- To review genetic biomarker-based approaches in NSCLC.
- To highlight the impact of EGFR and ALK alterations on treatment strategies.
- To emphasize the benefits of individualized therapy for NSCLC patients.
Main Methods:
- Review of literature on EGFR mutations and ALK rearrangements in NSCLC.
- Analysis of clinical data for targeted therapies (gefitinib, erlotinib, crizotinib).
- Focus on patient selection based on molecular genetic characterization.
Main Results:
- EGFR mutations confer high sensitivity to EGFR tyrosine kinase inhibitors, leading to superior response rates and progression-free survival in NSCLC.
- The EML4-ALK fusion oncogene is effectively targeted by crizotinib, showing greater efficacy than standard chemotherapy in NSCLC.
- Identification of these biomarkers enables precise patient stratification for targeted treatments.
Conclusions:
- Genetic biomarkers like EGFR mutations and ALK rearrangements are crucial for personalized NSCLC treatment.
- Targeted therapies have significantly improved clinical outcomes compared to traditional chemotherapy.
- Individualized therapy based on molecular profiling is the future of effective NSCLC management.
Related Concept Videos
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
Combination Therapies and Personalized Medicine
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
Modified-Release Drug Delivery Systems: Site-Targeted
Cancer Therapies
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...
