ArticleBritish journal of cancer1999
Non-autocrine, constitutive activation of Met in human anaplastic thyroid carcinoma cells in culture.
Article in British journal of cancer, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Overexpressed MET drives aggressive thyroid cancer phenotypes and serves as a precision therapeutic target.Scientific reports · 2025Article
- Anlotinib inhibits c-MET and ITGA2 in the treatment of anaplastic thyroid carcinoma.World journal of surgical oncology · 2025Article
- Genetic alterations in thyroid cancer mediating both resistance to BRAF inhibition and anaplastic transformation.Oncotarget · 2024Article
- Article
- Valproic acid, targets papillary thyroid cancer through inhibition of c-Met signalling pathway.American journal of translational research · 2017Article
- Off-target effects of c-MET inhibitors on thyroid cancer cells.Molecular cancer therapeutics · 2014Article
- Identification of the receptor tyrosine kinase c-Met and its ligand, hepatocyte growth factor, as therapeutic targets in clear cell sarcoma.Cancer research · 2010Article
- Distinct genetic alterations in the mitogen-activated protein kinase pathway dictate sensitivity of thyroid cancer cells to mitogen-activated protein kinase kinase 1/2 inhibition.Thyroid : official journal of the American Thyroid Association · 2009Article
- Planning for intracavitary anti-EGFR radionuclide therapy of gliomas. Literature review and data on EGFR expression.Journal of neuro-oncology · 2006Review
- Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- The transcriptional activator PAX3-FKHR rescues the defects of Pax3 mutant mice but induces a myogenic gain-of-function phenotype with ligand-independent activation of Met signaling in vivo.Genes & development · 2003Article
- Tyrosine kinase inhibitor STI571 enhances thyroid cancer cell motile response to Hepatocyte Growth Factor.Oncogene · 2001Article
- Expression of Hepatocyte Growth Factor (HGF) and its Receptor (MET) in Medullary Carcinoma of the Thyroid.Endocrine pathology · 2000Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of Met by its ligand HGF has been shown to elicit both mitogenic and motogenic responses in thyrocytes in vitro. In the present study we have investigated the expression of Met in human anaplastic thyroid carcinoma cells in culture. There was a variation in expression level and size of Met in the different cell lines; high Met expression was found in four cell lines, compared to non-neoplastic human thyrocytes. Treatment with glucoproteinase F showed that the size differences observed were due to variances in the degree of glycosylation. Interestingly, in cell lines with high expression of Met, the receptor proteins were found to be constitutively tyrosine phosphorylated. None of these cell lines expressed HGF mRNA, and addition of suramin did not affect the level of tyrosine phosphorylation of Met in unstimulated cells, suggesting the absence of autocrine stimulatory pathways. Furthermore, we did not observe MET gene amplification, activating mutations or phosphatase defects. The tyrosine phosphorylated receptors appeared functionally active since the receptors associated with the adaptor molecule Shc. In summary, we have found ligand-independent constitutively activated Met in four out of six anaplastic thyroid carcinoma cell lines.
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