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Your search keyword '"Marialuisa Sponziello"' showing total 2 results
Start Over Author "Marialuisa Sponziello" Publisher hindawi limited
2 results on '"Marialuisa Sponziello"'

1. Expression of Leptin Receptor and Effects of Leptin on Papillary Thyroid Carcinoma Cells

Author

Marilena Celano, Valentina Maggisano, Saverio Massimo Lepore, Marialuisa Sponziello, Valeria Pecce, Antonella Verrienti, Cosimo Durante, Marianna Maranghi, Piernatale Lucia, Stefania Bulotta, Giuseppe Damante, and Diego Russo

Subjects
Diseases of the endocrine glands. Clinical endocrinology, RC648-665
Abstract

Background. Obesity has been hypothesized to contribute to the aggressiveness of thyroid cancer through the production of abnormal levels of serum adipokines. Leptin receptor (OB-R) expression has also been documented in papillary thyroid cancer (PTC). Aim. In this translational study, we analyzed in vitro the effects of leptin on the growth and migration of thyroid cancer cells (TPC-1 and K1), the molecular mechanisms underlying leptin’s action, and the influence of prolonged leptin exposure on cell response to a protein kinase inhibitor lenvatinib. The expression levels of OB-R mRNA and protein were also investigated in vivo in a series of aggressive PTCs divided into two groups based on the presence of the BRAF mutation. Results. In TPC-1 and K1 cells, prolonged treatment with leptin (500 ng/ml for 96 h) resulted in a mild increase in the proliferation (about 20% over control only in K1 cells, p

Published
2019
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2. Whole exome sequencing identifies a germline MET mutation in two siblings with hereditary wild-type RET medullary thyroid cancer

Author

Antonella Verrienti, Ferdinando Marandino, Diego Russo, Paolo Fortina, Anna Rita Virzì, Valeria Pecce, Marialuisa Appetecchia, Alessandra Gentile, Francesca Rosignolo, Melissa Milan, Cosimo Durante, Silvia Benvenuti, Eric Londin, Paolo M. Comoglio, Agnese Barnabei, Marialuisa Sponziello, and Sebastiano Filetti

Subjects
Male, 0301 basic medicine, Proband, endocrine system diseases, RET proto-oncogene, Biology, medicine.disease_cause, medullary thyroid cancer, Proto-Oncogene Mas, Germline, whole exome sequencing, familial medullary thyroid cancer, MET proto-oncogene, Genetics, Genetics (clinical), 03 medical and health sciences, 0302 clinical medicine, Germline mutation, Exome Sequencing, Genotype, medicine, Humans, Thyroid Neoplasms, Exome sequencing, Mutation, Base Sequence, Siblings, Proto-Oncogene Proteins c-ret, Medullary thyroid cancer, Proto-Oncogene Proteins c-met, medicine.disease, Carcinoma, Neuroendocrine, Pedigree, Germ Cells, 030104 developmental biology, 030220 oncology & carcinogenesis, Cancer research, Female
Abstract

Whole exome sequencing (WES) was used to investigate two Italian siblings with wild-type RET genotype, who developed medullary thyroid cancers (MTCs) and, later, primary prostate and breast cancers, respectively. The proband's MTC harbored a p.Met918Thr RET mutation; his sister's MTC was RET/RAS wild-type. Both siblings had a germline mutation (p.Arg417Gln) in the extracellular Sema domain of the proto-oncogene MET. Experiments involving ectopic expression of MET p.Arg417Gln in MET-negative T47D breast cancer cells documented the mutant receptor's functionality and its ability to enhance cell migration and invasion. Our findings highlight a possible link between MET germline mutations and MTCs and suggest that MET p. Arg417Gln may promote an invasive malignant phenotype. The possibility that MTC can be driven/co-driven by a MET mutation has potential management implications, since the tyrosine-kinase inhibitor cabozantinib-approved for treating advanced MTCs-is a specific MET inhibitor.

Published
2017
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