Related Experiment Video
Updated: May 27, 2026

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 EGFR in non-small-cell lung cancer: lessons, experiences, strategies
Giulia M Stella1, Maurizio Luisetti, Simona Inghilleri
1Department of Hematological, Pneumological and Cardiovascular Sciences, Section of Pneumology, University and Fondazione IRCCS Policlinico, San Matteo, 27100 Pavia, Italy. g.stella@smatteo.pv.it
Abstract:
Cancer is a genetic disease and this concept is now widely exploited by both scientists and clinicians to design new targeted molecules. Indeed many data have already allowed us to ameliorate not only our knowledge about cancer onset, but also about patients treatment. Correlation between mutations in cancer alleles and drug response is a key point to identify drugs that match the genetic profile of each individual tumors. On the other hand, experience derived from inhibition of tyrosine kinase receptors has pointed out that targeted treatment is really successful only in a small subset of tumors. The latter are eventually addicted to those genetic alterations which are responsible for receptors activation and for the continued expression of their signalling. Overall these observations provide a strong rationale for a molecular-based diagnosis and patients selection for targeted therapies. This review analyses the current state of the art of molecularly-tailored pharmacological approach to lung cancer, one of the biggest killers among human solid tumors. Main relevance is addressed to genetic lesions activating the EGFR pathway transducers, focusing on their role as markers of targeted drug response.
Insights
Targeted cancer therapies are most effective when matched to a patient's genetic profile. This review focuses on genetic mutations in lung cancer, particularly those affecting the EGFR pathway, as key indicators for successful targeted drug response.
Area of Science:
- Oncology
- Pharmacogenomics
- Molecular Biology
Background:
- Cancer is fundamentally a genetic disease, driving research into targeted therapies.
- Understanding gene mutations is crucial for predicting patient response to cancer drugs.
- Targeted treatments, like tyrosine kinase receptor inhibitors, show success in specific tumor subsets dependent on particular genetic alterations.
Purpose of the Study:
- To review the current state of molecularly-tailored pharmacological approaches for lung cancer.
- To highlight the significance of genetic lesions in the EGFR pathway as predictive markers for targeted therapy response.
Main Methods:
- Literature review of molecularly-tailored pharmacological approaches in lung cancer.
- Analysis of genetic alterations, focusing on the EGFR pathway.
- Examination of the role of these genetic lesions as markers for targeted drug efficacy.
Main Results:
- Genetic profiling of tumors is essential for personalized cancer treatment.
- Specific mutations activating EGFR pathway transducers are strong indicators of targeted drug response in lung cancer.
- Targeted therapies are most effective in tumors with a genetic addiction to specific signaling pathways.
Conclusions:
- Molecular-based diagnosis and patient selection are critical for optimizing targeted lung cancer therapies.
- EGFR pathway genetic lesions serve as vital biomarkers for guiding treatment decisions.
- Personalized medicine approaches, informed by genetic data, represent the future of lung cancer treatment.
More Related Videos
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
05:17Detection of Targetable Alterations in Non-small Cell Lung Cancer using Next-generation Sequencing
Published on: October 10, 2025
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...
Mitogens and the Cell Cycle
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase