Related Experiment Video

Updated: May 1, 2026

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib
09:38

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib

Published on: June 26, 2019

7.6K

Overcoming T790M-driven acquired resistance to EGFR-TKIs in NSCLC with afatinib: a case report

Paola Bordi, Marcello Tiseo, Beatrice Bortesi

    Tumori
    |March 29, 2014
    PubMed

    Insights

    Acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer (NSCLC) is a challenge. Afatinib showed significant response in a T790M-positive NSCLC patient, highlighting potential but also limitations in brain metastases.

    Area of Science:

    • Oncology
    • Molecular Biology
    • Pharmacology

    Background:

    • Activating EGFR mutations significantly alter non-small cell lung cancer (NSCLC) progression.
    • Targeted therapies like gefitinib and erlotinib have improved outcomes for EGFR-mutated NSCLC.
    • Acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) remains a critical clinical challenge.

    Observation:

    • A patient with metastatic EGFR-mutated NSCLC developed T790M-mediated acquired resistance to TKIs.
    • The patient was treated with afatinib, a fourth-generation EGFR TKI.

    Findings:

    • Afatinib treatment resulted in a significant overall response across multiple disease sites.
    • The response to afatinib was notably limited in brain metastases.
    • This case represents the first reported instance of afatinib efficacy in T790M-driven acquired resistance in NSCLC.

    Implications:

    • Afatinib demonstrates potential in overcoming T790M-mediated acquired resistance in EGFR-mutated NSCLC.
    • The limited efficacy on brain metastases suggests further investigation into afatinib's role in CNS disease is warranted.
    • This case contributes to understanding resistance mechanisms and optimizing treatment strategies for advanced NSCLC.

    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

    8.0K
    A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds13:34

    A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds

    Published on: April 6, 2016

    9.5K

    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...
    2.6K
    Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

    Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

    Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
    81