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

Activation of MET by gene amplification or by splice mutations deleting the juxtamembrane domain in primary resected lung cancers.

Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer - 1 Jan 2009

Onozato Ryoichi, Kosaka Takayuki, Kuwano Hiroyuki, Sekido Yoshitaka, Yatabe Yasushi, Mitsudomi Tetsuya

Abstract excerpt

INTRODUCTION: MET (Met proto-oncogene) activation either by gene amplification or mutation is implicated in various types of human cancers. For lung cancer, MET gene amplification is reported to occur in a subset of adenocarcinomas. Although somatic mutations of MET in lung adenocarcinomas are ra...

Read the complete abstract on PubMed

Topics

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

Share to Carcinoma, Adenosquamous
Share to Carcinoma, Large Cell

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Pneumonectomy

Share to Proto-Oncogene Mas

Share to Proto-Oncogene Proteins c-cbl

Share to Proto-Oncogene Proteins c-met

Share to Receptors, Growth Factor

Share to Small Cell Lung Carcinoma

Source

Identifiers

PMID: 19096300
DOI: 10.1097/JTO.0b013e3181913e0e

Genes

MET
KRAS

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-19096300-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Activation of MET by gene amplification or by splice mutations deleting the juxtamembrane domain in primary resected lung cancers.PMID 19096300Read ↗

MET amplification, protein expression, and mutations in pulmonary adenocarcinoma.Semantic proximity Read ↗

MET exon 14 juxtamembrane splicing mutations: clinical and therapeutical perspectives for cancer therapySemantic proximity Read ↗

MET alterations in advanced pulmonary sarcomatoid carcinomaSemantic proximity Read ↗

The METeoric rise of MET in lung cancerSemantic proximity Read ↗

Gastric cancer cell line Hs746T harbors a splice site mutation of c-Met causing juxtamembrane domain deletion.Semantic proximity Read ↗

Identification of MET fusions as novel therapeutic targets sensitive to MET inhibitors in lung cancer.Semantic proximity Read ↗

Somatic mutations lead to an oncogenic deletion of met in lung cancer.Semantic proximity Read ↗

MET Amplification and Exon 14 Splice Site Mutation Define Unique Molecular Subgroups of Non-Small Cell Lung Carcinoma with Poor Prognosis.Semantic proximity Read ↗

MET Exon 14 Mutation Encodes an Actionable Therapeutic Target in Lung Adenocarcinoma.Semantic proximity Read ↗

Characterization of 298 Patients with Lung Cancer Harboring MET Exon 14 Skipping Alterations.Semantic proximity Read ↗

MET exon 14 skipping defines a unique molecular class of non-small cell lung cancer.Semantic proximity Read ↗

MET Gene Amplification and Overexpression in Chinese Non-Small-Cell Lung Cancer Patients Without EGFR Mutations.Semantic proximity Read ↗

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