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Your search keyword '"Castellone, M. D"' showing total 4 results
Start Over Author "Castellone, M. D" Topic thyroid neoplasms
4 results on '"Castellone, M. D"'

1. Genetic alterations in differentiated thyroid cancer: what can be expected for gene expression profiling of thyroid carcinomas.

Author

Santoro M, Melillo RM, Carlomagno F, Castellone MD, Vitagliano D, Guida T, Vecchio G, and Fusco A

Subjects
Animals, Carcinoma, Papillary genetics, Humans, Mutation, Oncogene Proteins genetics, Proto-Oncogene Proteins c-ret, Receptor Protein-Tyrosine Kinases genetics, Receptor, trkA genetics, Gene Expression Profiling, Thyroid Neoplasms genetics
Published
2003

2. RET/PTC1 oncogene signaling in PC Cl 3 thyroid cells requires the small GTP-binding protein Rho.

Author

Barone MV, Sepe L, Melillo RM, Mineo A, Santelli G, Monaco C, Castellone MD, Tramontano D, Fusco A, and Santoro M

Subjects
3T3 Cells, Actins metabolism, Adenocarcinoma pathology, Animals, Apoptosis, Breast Neoplasms pathology, Cell Line, Cell Line, Transformed, Cell Survival, DNA Replication, Dimerization, Female, Humans, MAP Kinase Signaling System, Membrane Proteins genetics, Membrane Proteins metabolism, Mice, Multiple Endocrine Neoplasia Type 2a genetics, Multiple Endocrine Neoplasia Type 2a metabolism, Neoplasm Invasiveness, Neoplasm Proteins metabolism, Organ Specificity, Phenotype, Protein-Tyrosine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-ret, Rats, Receptor Protein-Tyrosine Kinases, Recombinant Fusion Proteins physiology, Transfection, Tumor Cells, Cultured, Carcinoma, Papillary pathology, Drosophila Proteins, Oncogene Proteins, Fusion physiology, Signal Transduction physiology, Stress Fibers physiology, Thyroid Gland cytology, Thyroid Neoplasms pathology, rho GTP-Binding Proteins physiology
Abstract

Thyroid papillary carcinomas are characterized by RET/PTC rearrangements that cause the tyrosine kinase domain of the RET receptor to fuse with N-terminal sequences encoded by heterologous genes. This results in the aberrant expression of a ligand-independent and constitutively active RET kinase. We analysed actin reorganization induced by the RET/PTC1 oncogene in PC Cl 3 rat thyroid epithelial cells. Differently from oncogenes Src, Ras and Raf, RET/PTC1 caused actin filaments to form prominent stress fibers. Moreover, stress fibers were identified in human thyroid papillary carcinoma cell lines harboring RET/PTC1 rearrangements but not in thyroid carcinoma cells negative for RET/PTC rearrangements. RET/MEN 2A, a constitutively active but unrearranged membrane-bound RET oncoprotein, did not induce stress fibers in PC Cl 3 cells. Induction of stress fibers by RET/PTC1 was restricted to thyroid cells; it did not occur in NIH3T3 fibroblasts or MCF7 mammary cells. RET/PTC1-mediated stress fiber formation depended on Rho but not Rac small GTPase activity. In addition, inhibition of Rho, but not of Rac, caused apoptosis of RET/PTC1-expressing thyroid cells. We conclude that Rho is implicated in the actin reorganization and cell survival mediated by the chimeric RET/PTC1 oncogene in thyroid epithelial cells, both phenotypes being cell type- and oncogene type-specific.

Published
2001
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3. Genetic alterations in differentiated thyroid cancer: what can be expected for gene expression profiling of thyroid carcinomas

Author

Santoro, M., Rosa Marina MELILLO, Carlomagno, F., Castellone, M. D., Vitagliano, D., Guida, T., Vecchio, G., Fusco, A., Santoro, Massimo, Melillo, ROSA MARINA, Carlomagno, Francesca, Castellone, MARIA DOMENICA, Vitagliano, Donata, Guida, Teresa, Vecchio, Giancarlo, and Fusco, Alfredo

Subjects
Oncogene Proteins, Gene Expression Profiling, Mutation, Proto-Oncogene Proteins c-ret, Animals, Humans, Receptor Protein-Tyrosine Kinases, Thyroid Neoplasms, Receptor, trkA, Carcinoma, Papillary
Published
2003

4. Functional expression of the CXCR4 chemokine receptor is induced by RET/PTC oncogenes and is a common event in human papillary thyroid carcinomas

Author

Pinuccia Faviana, Maria Domenica Castellone, Rosa Marina Melillo, Francesca Carlomagno, Torben F. Ørntoft, John P Russell, Mogens Kruhøffer, Fulvio Basolo, Massimo Santoro, Jay L. Rothstein, Alfredo Fusco, Valentina De Falco, Valentina Guarino, Castellone, M. D., Guarino, V., DE FALCO, V., Carlomagno, Francesca, Basolo, F., Faviana, P., Kruhoffer, M., Orntoft, T., Russell, J. P., Rothstein, J. L., Fusco, Alfredo, Santoro, Massimo, and Melillo, ROSA MARINA

Subjects
Cancer Research, endocrine system, Receptors, CXCR4, endocrine system diseases, Chemokine receptor, Cell Survival, Biology, medicine.disease_cause, S Phase, Thyroid hormone receptor beta, Thyroid carcinoma, Proto-Oncogene Proteins, Genetics, medicine, Humans, Neoplasm Invasiveness, Thyroid Neoplasms, RET/PTC oncogenes, Molecular Biology, Thyroid hormone receptor, Chemotaxis, Thyroid, Proto-Oncogene Proteins c-ret, Receptor Protein-Tyrosine Kinases, Oncogenes, Carcinoma, Papillary, Chemokine CXCL12, Gene Expression Regulation, Neoplastic, medicine.anatomical_structure, Cancer research, Ectopic expression, Carcinogenesis, PAX8, Thyroid tumor, Chemokines, CXC, Signal Transduction
Abstract

To identify genes involved in the transformation of thyroid follicular cells, we explored, using DNA oligonucleotide microarrays, the transcriptional response of PC Cl3 rat thyroid epithelial cells to the ectopic expression of the RET/PTC oncogenes. We found that RET/PTC was able to induce the expression of CXCR4, the receptor for the chemokine CXCL12/SDF-1alpha/beta. We observed that CXCR4 expression correlated with the transforming ability of the oncoprotein and depended on the integrity of the RET/PTC-RAS/ERK signaling pathway. We found that CXCR4 was expressed in RET/PTC-positive human thyroid cancer cell lines, but not in normal thyroid cells. Furthermore, we found CXCR4 expression in human thyroid carcinomas, but not in normal thyroid samples by immunohistochemistry. Since CXCR4 has been recently implicated in tumor proliferation, motility and invasiveness, we asked whether treatment with SDF-1alpha was able to induce a biological response in thyroid cells. We observed that SDF-1alpha induced S-phase entry and survival of thyroid cells. Invasion through a reconstituted extracellular matrix was also supported by SDF-1alpha and inhibited by a blocking antibody to CXCR4. Taken together, these results suggest that human thyroid cancers bearing RET/PTC rearrangements may use the CXCR4/SDF-1alpha receptor-ligand pathway to proliferate, survive and migrate.

Published
2004
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