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

Non-small cell lung cancer harboring EGFR G724S mutation and exon 19 deletion responded to afatinib monotherapy after multiple lines of target therapies.

Anti-cancer drugs - 1 Oct 2022

Cortiula Francesco, Pelizzari Giacomo, Corvaja Carla, De Maglio Giovanna, Fasola Gianpiero

Abstract excerpt

Epidermal growth factor receptor (EGFR) G724S mutation represents a resistance mechanism to first- and third-generation EGFR tyrosine kinase inhibitors. Limited data are available regarding the efficacy of afatinib in patients with non-small cell lung cancer (NSCLC) harboring G724S mutation, particularly after osimertinib. A patient diagnosed with advanced EGFR-mutated (exon 19 deletion) NSCLC after several lines...

Read the complete abstract on PubMed

Topics

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

Share to Acrylamides
Share to Afatinib

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Aniline Compounds

Share to Gefitinib

Share to Heat-Shock Proteins

Share to Indoles

Share to Protein Kinase Inhibitors

Share to Pyrimidines

Source

Open in PubMed Open full text

Identifiers

PMID: 35979997
DOI: 10.1097/CAD.0000000000001321
PMCID: PMC9481291

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

Non-small cell lung cancer harboring EGFR G724S mutation and exon 19 deletion responded to afatinib monotherapy after multiple lines of target therapies.PMID 35979997Read ↗

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 ↗

EGFR exon 18 delE709_T710insD mutated stage IV non-small cell lung cancer treated with osimertinib: a case report.Semantic proximity Read ↗

Characterization of a rare EGFR resistance mutation in a lung cancer patient with a long response to osimertinib: case report.Semantic proximity Read ↗

Successful treatment of an osimertinib-resistant lung adenocarcinoma with an exon 18 EGFR mutation (G719S) with afatinib plus bevacizumab.Semantic proximity Read ↗

EGFR exon 19 deletion switch and development of p.L792Q mutation as a new resistance mechanism to osimertinib: a case report and literature reviewSemantic proximity Read ↗

Afatinib treatment in a lung adenocarcinoma patient harboring a rare EGFR L747P mutation.Semantic proximity Read ↗

Dacomitinib overcomes afatinib-refractory carcinomatous meningitis in a lung cancer patient harbouring EGFR Ex.19 deletion and G724S mutation; A case reportSemantic proximity Read ↗

On-target Resistance to the Mutant-Selective EGFR Inhibitor Osimertinib Can Develop in an Allele-Specific Manner Dependent on the Original EGFR-Activating MutationSemantic proximity Read ↗

Durable response to afatinib rechallenge in a long-term survivor of non-small cell lung cancer harboring EGFR L858R and L747V mutations.Semantic proximity Read ↗

Novel EGFR Exon 18 (G721R) Mutation in a Patient with Non-Small Cell Lung Carcinoma with Lack of Response to Afatinib.Semantic proximity Read ↗

Successful Treatment of Afatinib Reversing Epidermal Growth Factor Receptor Exon19Deletion/G724S Mutation Resistance Guided by Protein-Drug Docking.Semantic proximity Read ↗

Overcoming EGFRG724S-mediated osimertinib resistance through unique binding characteristics of second-generation EGFR inhibitorsSemantic proximity Read ↗

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