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 - Development of Parallel Mechanisms of Resistance].

Pneumologie (Stuttgart, Germany) - 1 Jul 2018

Moeller M, Siebolts U, Wickenhauser C, Schuette W

Abstract excerpt

Acquired resistances to tyrosine kinase inhibitors in non-small cell lung cancer develop after 9 - 12 month. In 60 % of the cases these resistances arise because of a secondary EGFR-T790 M resistance mutation. This report is describing the case of a patient who developed parallel two different mechanisms of resistance: A T790 M resistance mutation and a transformation into a small cell neuroendocrine cancer....

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
Share to Carboplatin

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

Share to Carcinoma, Neuroendocrine

Share to Drug Resistance, Neoplasm

Share to Etoposide

Share to Piperazines

Share to Protein Kinase Inhibitors

Source

Identifiers

PMID: 29466812
DOI: 10.1055/s-0044-100192

Genes

EGFR

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. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 10 closest

[Non-Small Cell Lung Cancer - Development of Parallel Mechanisms of Resistance].PMID 29466812Read ↗

Large Cell Neuroendocrine Carcinoma Transformation and EGFR-T790M Mutation as Coexisting Mechanisms of Acquired Resistance to EGFR-TKIs in Lung Cancer.Semantic proximity Read ↗

Heterogeneous resistance mechanisms in an EGFR exon 19-mutated non-small cell lung cancer patient treated with erlotinib: Persistent FGFR3-mutation, localized transformation to EGFR-mutated SCLC, and acquired T790M EGFR-mutation.Semantic proximity Read ↗

Simultaneous Acquisition of T790M Mutation and SCLC Transformation during Targeted Therapy in EGFR-Mutated Lung Adenocarcinoma: A Rare Case Report.Semantic proximity Read ↗

[Resistances to targeted therapies and strategy for following therapeutic lines in metastatic NSCLC].Semantic proximity Read ↗

[Management of patients with resistance to EGFR-TKI].Semantic proximity Read ↗

Small-cell lung cancer transformation from EGFR-mutant adenocarcinoma after EGFR-TKIs resistance: A case report.Semantic proximity Read ↗

Transformation to small cell lung cancer as an acquired resistance mechanism in EGFR-mutant lung adenocarcinoma: a case report of complete response to etoposide and cisplatin.Semantic proximity Read ↗

Transformation to "high grade" neuroendocrine carcinoma as an acquired drug resistance mechanism in EGFR-mutant lung adenocarcinoma.Semantic proximity Read ↗

[Patient with Three EGFR Mutations - Gradual Development of Resistance to Previous Targeted Treatment].Semantic proximity Read ↗

Acquired resistance of pulmonary adenocarcinoma to initially successful targeted therapy due to EGFR mutation T790M.Semantic proximity Read ↗

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