ArticleCancer science2007
c-Met activation in lung adenocarcinoma tissues: an immunohistochemical analysis.
Article in Cancer science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed, 3 syntheses or guidelines pooled it, 140 citations in OpenAlex.
- Pooled it
- Pooled it
- International association for the study of lung cancer/american thoracic society/european respiratory society international multidisciplinary classification of lung adenocarcinoma.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2011Pooled it
- Immunological effects of amivantamab in EGFR or MET-expressing non-small cell lung cancer.Cancer immunology, immunotherapy : CII · 2026Article
- Article
- MET Overexpression Is Associated with Superior Immunotherapy Benefit in Advanced Non-Small Cell Lung Cancer.Cancers · 2025Article
- MET (c-Met) protein overexpression is an emerging protein biomarker in non-small cell lung cancer.NPJ precision oncology · 2025Review
- MET Alterations in Cancer and MET-Targeted Therapy: Detection Strategies, Treatment Efficacy, and Emerging Technologies.Targeted oncology · 2025Review
- HGF/c-Met/β1-integrin signalling axis induces tunneling nanotubes in A549 lung adenocarcinoma cells.Life science alliance · 2023Article
- MET in Non-Small-Cell Lung Cancer (NSCLC): Cross 'a Long and Winding Road' Looking for a Target.Cancers · 2023Review
- Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth.International journal of cancer · 2023Article
- Preclinical Profile of BYON3521 Predicts an Effective and Safe MET Antibody-Drug Conjugate.Molecular cancer therapeutics · 2023Article
- MET-targeted therapies for the treatment of non-small-cell lung cancer: A systematic review and meta-analysis.Frontiers in oncology · 2022Review
- Article
- Non-Small Cell Lung Cancer from Genomics to Therapeutics: A Framework for Community Practice Integration to Arrive at Personalized Therapy Strategies.Journal of clinical medicine · 2020Review
- MET targeting: time for a rematch.Oncogene · 2020Review
- Prevalence and Clinicopathological Significance of MET Overexpression and Gene Amplification in Patients with Gallbladder Carcinoma.Cancer research and treatment · 2020Article
- The Emerging Role of the c-MET-HGF Axis in Non-small Cell Lung Cancer Tumor Immunology and Immunotherapy.Frontiers in oncology · 2020Review
- Significance of PD-L1 clones and C-MET expression in hepatocellular carcinoma.Oncology letters · 2019Article
- The multiple paths towards MET receptor addiction in cancer.Oncogene · 2018Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-Met is often overexpressed in non-small cell lung cancer, but it remains unsolved whether its overexpression leads to its activation. We used an antibody specific to phospho-c-Met (Tyr1235) to investigate c-Met activation immunohistochemically in 130 surgically resected lung adenocarcinomas. The expression of c-Met and hepatocyte growth factor (HGF) was also investigated. Phospho-c-Met was positive in 21.5% (28/130) of cases. c-Met was positive in 74.6% of cases (97/130) and was expressed at high levels in 36.1% of cases (47/130). HGF was expressed at high levels in 31.5% of cases (41/130). Phospho-c-Met was correlated with high levels of HGF (P =0.0010) and high levels c-Met expression (P = 0.0303), but it was also found to be positive in 12 cases with little to no HGF expression. Phospho-c-Met expression was significantly associated with tumor differentiation (P = 0.0023) and papillary histology (P = 0.0011), but not with pathological stage, lymph node metastasis or survival. High levels of c-Met and HGF were also associated with papillary histology (P = 0.0056 and P = 0.0396, respectively), but not with tumor differentiation. Phospho-c-Met was correlated with phospho-Akt (P = 0.0381), but not with phospho-Erk or phospho-Stat3. Phospho-Akt expression was marginally correlated with the expression of phospho-epidermal growth factor receptor (EGFR) (P = 0.0533) and, importantly, it was strongly correlated with the expression of either phospho-c-Met or phospho-EGFR (P = 0.0013). The data suggest that in lung adenocarcinoma tissue, c-Met activation may take place either ligand-dependently or ligand-independently via c-Met overexpression. c-Met activation may play special roles in the papillary subtype and in well differentiated lung adenocarcinomas.
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Registered trials
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