Overexpression of the C-MET/HGF receptor in human thyroid carcinomas derived from the follicular epithelium

Renzo, Maria Flavia Di; Olivero, Martina; Serini, Guido; Orlandi, Fabio; Pilotti, Silvana; Belfiore, Antonino; Costantino, Angela; Vigneri, Riccardo; Angeli, A; Pierotti, Marco A.; Comoglio, Paolo M.

doi:10.1007/bf03349722

Cited by 172 publications

(194 citation statements)

References 32 publications

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“…The presence of high amounts of receptors on the cell surface (overexpression) favors homodimerization and receptor activation (Heldin, 1995). This could explain why overexpression induces constitutive activation of Met and Ron kinases in vitro (Giordano et al, 1988b;Gaudino et al, 1994) and in several human tumors (Di Renzo et al, 1995;Natali et al, 1996;Maggiora et al, 1998;Taniguchi et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Cross-talk between the proto-oncogenes Met and Ron

et al. 2000

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Section: Discussionmentioning

confidence: 99%

Cross-talk between the proto-oncogenes Met and Ron

et al. 2000

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“…Furthermore, studies for the expression pattern in normal, premalignant and malignant lesions has demonstrated overexpression of the c-MET gene in different tumors. [53][54][55][56] HGF/SF is produced by several epithelial tumors. 57,58 Production of HGF/SF by breast cancer cells, measured either in serum of patients or in tumor extracts, is an indicator of aggressive behavior of the tumor.…”

Section: Discussionmentioning

confidence: 99%

Hepatocyte growth factor/scatter factor (HGF/SF) affects proliferation and migration of myeloid leukemic cells

et al. 1998

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Hepatocyte growth factor (HGF), also known as scatter factor (SF), is produced by mesenchymal cells, including bone marrow (BM) stromal cells, and has mitogenic and motogenic effects on a variety of cell types. Recently, a role has been assigned to HGF/SF and its receptor, c-MET, in both normal and malignant hemopoiesis. We investigated the function of HGF/SF on hemopoietic mononuclear cells (MNC) from patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) with circulating blasts. In contrast to results with normal MNC, HGF/SF alone stimulated the proliferation and colony formation of MNC from these patients. MNC from some (4/13) of the AML patients also produced HGF/SF (0.1-0.2 ng/ml/day), while we could not detect HGF/SF in cultures from normal MNC. Furthermore, it appeared that HGF/SF induced migration of leukemic cells in Boyden using KG1a cells as a model for leukemic blasts. The membranes dividing the two compartments of the Boyden chambers were coated with fibronectin. HGF/SF significantly promoted migration in 3/5 samples of MDS patients and in 5/7 samples of AML patients. Supernatant of human BM stromal cells, which is chemoattractive for normal human hemopoietic progenitor cells, also promoted migration of MNC from 4/5 MDS patients and 6/7 AML patients. Since HGF/SF is one of the growth factors produced by BM stromal cells, a neutralizing antibody directed against HGF/SF was added to the BM stroma supernatant, which reduced migration significantly in 2/3 MDS and in 3/6 AML responders to BM stroma supernatant. In conclusion, HGF/SF promotes proliferation and migration of hemopoietic cells from AML and MDS patients in vitro and may therefore contribute to the malignant potential of these cells.

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“…In PTC, overexpression of c-Met has been found in 70% of patients (Di Renzo et al 1992), and ATC is associated with constitutively active c-Met as well (Bergstrom et al 1999). In PTC, high levels of c-Met expression correlate inversely with the presence of distant metastasis (Belfiore et al 1997).…”

Section: Novel Insights In the Pathogenesis Of Thyroid Cancermentioning

confidence: 99%

New therapeutic advances in the management of progressive thyroid cancer

Woyach¹,

Shah²

2009

Endocrine-Related Cancer

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The spectrum of thyroid cancers ranges from one of the most indolent to one of the most aggressive solid tumors identified. Conventional therapies for thyroid cancers are based on the histologic type of thyroid cancers such as papillary or follicular thyroid cancer (differentiated thyroid cancer (DTC)), medullary thyroid cancer (MTC), or anaplastic thyroid cancer (ATC). While surgery is one of the key treatments for all such types of thyroid cancers, additional therapies vary. Effective targeted therapy for DTC is a decades-old practice with systemic therapies of thyroid stimulating hormone suppression and radioactive iodine therapy. However, for the iodinerefractory DTC, MTC, and ATC there is no effective systemic standard of care treatment. Recent advances in understanding pathogenesis of DTC and development of molecular targeted therapy have dramatically transformed the field of clinical research in thyroid cancer. Over the last five years, incredible progress has been made and phases I-III clinical trials have been conducted in various types of thyroid cancers with some remarkable results that has made an impact on lives of patients with thyroid cancer. Such history-making events have boosted enthusiasm and interest among researchers, clinicians, patients, and sponsors and we anticipate ongoing efforts to develop more effective and safe therapies for thyroid cancer.

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Overexpression of the C-MET/HGF receptor in human thyroid carcinomas derived from the follicular epithelium

Cited by 172 publications

References 32 publications

Cross-talk between the proto-oncogenes Met and Ron

Cross-talk between the proto-oncogenes Met and Ron

Hepatocyte growth factor/scatter factor (HGF/SF) affects proliferation and migration of myeloid leukemic cells

New therapeutic advances in the management of progressive thyroid cancer

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