Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Genomic landscape of acquired resistance to third-generation EGFR tyrosine kinase inhibitors in EGFR T790M-mutant non-small cell lung cancer.

Cancer - 1 Jun 2020

Lee Jiyun, Kim Hong Sook, Lee Boram, Kim Hee Kyung, Sun Jong-Mu, Ahn Jin Seok, Ahn Myung-Ju, Park Keunchil, Lee Se-Hoon

Abstract excerpt

BACKGROUND: EGFR tyrosine kinase inhibitors (TKIs) have shifted the treatment paradigm in advanced EGFR-mutant non-small cell lung cancer (NSCLC). However, patients who are treated with TKIs inevitably develop acquired resistance by mechanisms that are not fully understood. The purpose of this study was to investigate the mechanism of acquired resistance after treatment with third-generation EGFR TKIs. METHODS:...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acrylamides
Share to Aniline Compounds

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Carcinoma, Non-Small-Cell Lung

Share to Drug Resistance, Neoplasm

Share to ErbB Receptors

Share to Piperazines

Share to Protein Kinase Inhibitors

Share to Pyrimidines

Source

Identifiers

PMID: 32154925
DOI: 10.1002/cncr.32809

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genomic landscape of acquired resistance to third-generation EGFR tyrosine kinase inhibitors in EGFR T790M-mutant non-small cell lung cancer.PMID 32154925Read ↗

Exploring the resistance mechanisms of second-line osimertinib and their prognostic implications using next-generation sequencing in patients with non-small-cell lung cancer.Semantic proximity Read ↗

Acquired resistance to osimertinib in patients with non-small-cell lung cancer: mechanisms and clinical outcomes.Semantic proximity Read ↗

Investigating Novel Resistance Mechanisms to Third-Generation EGFR Tyrosine Kinase Inhibitor Osimertinib in Non-Small Cell Lung Cancer Patients.Semantic proximity Read ↗

Candidate mechanisms of acquired resistance to first-line osimertinib in EGFR-mutated advanced non-small cell lung cancer.Semantic proximity Read ↗

Acquired EGFR L718V mutation mediates resistance to osimertinib in non-small cell lung cancer but retains sensitivity to afatinib.Semantic proximity Read ↗

Next-generation sequencing reveals novel resistance mechanisms and molecular heterogeneity in EGFR-mutant non-small cell lung cancer with acquired resistance to EGFR-TKIs.Semantic proximity Read ↗

Tackling Osimertinib Resistance in EGFR-Mutant Non-Small Cell Lung Cancer.Semantic proximity Read ↗

Next-generation sequencing based mutation profiling reveals heterogeneity of clinical response and resistance to osimertinib.Semantic proximity Read ↗

Assessment of Resistance Mechanisms and Clinical Implications in Patients With EGFR T790M–Positive Lung Cancer and Acquired Resistance to OsimertinibSemantic proximity Read ↗

Analysis of acquired resistance mechanisms to osimertinib in patients with EGFR-mutated advanced non-small cell lung cancer from the AURA3 trial.Semantic proximity Read ↗

Rare Mechanism of Acquired Resistance to Osimertinib in Korean Patients with EGFR-mutated Non-small Cell Lung Cancer.Semantic proximity Read ↗

Newly emergent acquired EGFR exon 18 G724S mutation after resistance of a T790M specific EGFR inhibitor osimertinib in non-small-cell lung cancer: a case reportSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.