Related Experiment Video
Updated: May 10, 2026

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib
Published on: June 26, 2019
[Advanced research on T790M mutation in non-small cell lung cancer]
Hui Li1, Shuang Zhang, Ying Cheng
1Department of Thoracic Oncology, Jilin Provincial Cancer Hospital, Changchun 130012, China.
Abstract:
Patients with advanced non-small cell lung cancer (NSCLC) carrying epidermal growth factor receptor (EGFR) activating mutations benefit from EGFR-tyrosine kinase inhibitor (TKI) treatment, however, most of TKI-treated patients eventually suffer drug resistant after 10-month treatments. Previous studies demonstrated that T790M mutation in exon 20 of EGFR gene would be the essential factor leading to EGFR-TKI resistance, leaving the mechanisms of which elucidative. Current research identified that T790M is an independent, favorable prognostic factor for predicting survival, but whether it is also a predictive biomarker for EGFR-TKI efficacy is still controversial. Up to date, techniques to detect T790M mutation in lung cancer have been greatly improved and the new therapeutic strategies emerged as well. In this review, we summarized the newly updated data about T790M mutation in terms of its mechanisms involved in EGFR-TKI resistant, clinical value, advanced detection assays and ongoing strategies against the mutation subtype.
Insights
The T790M mutation in epidermal growth factor receptor (EGFR) drives resistance to EGFR-tyrosine kinase inhibitor (TKI) therapy in non-small cell lung cancer (NSCLC). This review covers T790M's role, detection, and new treatment strategies.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Advanced non-small cell lung cancer (NSCLC) patients with activating epidermal growth factor receptor (EGFR) mutations benefit from EGFR-tyrosine kinase inhibitor (TKI) therapy.
- Acquired resistance to EGFR-TKI treatment, often occurring within 10 months, is a significant clinical challenge in NSCLC management.
- The T790M mutation in exon 20 of the EGFR gene is identified as a primary mechanism conferring EGFR-TKI resistance.
Purpose of the Study:
- To review and summarize updated information on the T790M mutation in EGFR.
- To elucidate the mechanisms by which T790M contributes to EGFR-TKI resistance.
- To discuss the clinical significance, diagnostic advancements, and therapeutic strategies targeting T790M.
Main Methods:
- Literature review of recent studies on EGFR T790M mutation in NSCLC.
- Analysis of data regarding the role of T790M in EGFR-TKI resistance mechanisms.
- Evaluation of current and emerging diagnostic techniques and therapeutic approaches for T790M-positive NSCLC.
Main Results:
- T790M mutation is a key factor in EGFR-TKI resistance, though its precise mechanisms require further elucidation.
- T790M is recognized as an independent prognostic factor for survival in NSCLC patients.
- The predictive value of T790M for EGFR-TKI efficacy remains a subject of ongoing debate and research.
Conclusions:
- Significant advancements have been made in detecting the T790M mutation in lung cancer.
- New therapeutic strategies are emerging to overcome resistance mediated by the T790M mutation.
- Understanding T790M's role is crucial for optimizing treatment and improving outcomes for NSCLC patients.
