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Nose, Vania

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Nose

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Vania

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Nose, Vania
Author's Publications: search.filters.isAuthorOfPublication.be5e24ed-9c36-4ebd-a5c5-613c1418b026

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Now showing 1 - 4 of 4
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    Noninvasive Follicular Thyroid Neoplasm With Papillary-Like Nuclear Features (NIFTP): Achieving Better Agreement By Refining Diagnostic Criteria
    (Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, 2018) Alves, Venancio A.F.; Kakudo, Kennichi; LiVolsi, Virginia; Lloyd, Ricardo V.; Nikiforov, Yuri E.; Nose, Vania; Papotti, Mauro; Thompson, Lester D.R.
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    Metastasis-associated MCL1 and P16 copy number alterations dictate resistance to vemurafenib in a BRAFV600E patient-derived papillary thyroid carcinoma preclinical model
    (Impact Journals LLC, 2015) Duquette, Mark; Sadow, Peter; Husain, Amjad; Sims, Jennifer N.; Antonello, Zeus A.; Fischer, Andrew H.; Song, Chen; Castellanos-Rizaldos, Elena; Makrigiorgos, Gerassimos; Kurebayashi, Junichi; Nose, Vania; Van Hummelen, Paul; Bronson, Roderick; Vinco, Michelle; Giordano, Thomas J.; Dias-Santagata, Dora; Pandolfi, Pier Paolo; Nucera, Carmelo
    BRAFV600E mutation exerts an essential oncogenic function in many tumors, including papillary thyroid carcinoma (PTC). Although BRAFV600E inhibitors are available, lack of response has been frequently observed. To study the mechanism underlying intrinsic resistance to the mutant BRAFV600E selective inhibitor vemurafenib, we established short-term primary cell cultures of human metastatic/recurrent BRAFV600E-PTC, intrathyroidal BRAFV600E-PTC, and normal thyroid (NT). We also generated an early intervention model of human BRAFV600E-PTC orthotopic mouse. We find that metastatic BRAFV600E-PTC cells elicit paracrine-signaling which trigger migration of pericytes, blood endothelial cells and lymphatic endothelial cells as compared to BRAFWT-PTC cells, and show a higher rate of invasion. We further show that vemurafenib therapy significantly suppresses these aberrant functions in non-metastatic BRAFV600E-PTC cells but lesser in metastatic BRAFV600E-PTC cells as compared to vehicle treatment. These results concur with similar folds of down-regulation of tumor microenvironment–associated pro-metastatic molecules, with no effects in BRAFWT-PTC and NT cells. Our early intervention preclinical trial shows that vemurafenib delays tumor growth in the orthotopic BRAFWT/V600E-PTC mice. Importantly, we identify high copy number gain of MCL1 (chromosome 1q) and loss of CDKN2A (P16, chromosome 9p) in metastatic BRAFV600E-PTC cells which are associated with resistance to vemurafenib treatment. Critically, we demonstrate that combined vemurafenib therapy with BCL2/MCL1 inhibitor increases metastatic BRAFV600E-PTC cell death and ameliorates response to vemurafenib treatment as compared to single agent treatment. In conclusion, short-term PTC and NT cultures offer a predictive model for evaluating therapeutic response in patients with PTC. Our PTC pre-clinical model suggests that combined targeted therapy might be an important therapeutic strategy for metastatic and refractory BRAFV600E-positive PTC.
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    Ossifying Parotid Carcinoma ex Pleomorphic Adenoma
    (Hindawi Publishing Corporation, 2015) Mohan, Suresh; Puram, Sidharth; Yarlagadda, Bharat; Nose, Vania; Deschler, Daniel
    We present a unique case of an extensively ossified carcinoma ex pleomorphic adenoma (CXPA) in a 76-year-old man with a five-year history of a slowly growing parotid mass. Fine-needle aspiration of the mass was nondiagnostic. A computed tomography (CT) scan of the lesion revealed a well-circumscribed mass with peripheral calcification. Initial pathological analysis suggested a benign parotid mass, but rigorous decalcification revealed noninvasive CXPA. The patient underwent complete resection of the mass and remained disease-free nine months later. Extensive ossification of a seemingly benign parotid mass may mask areas of carcinoma that may progress if left untreated.
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    SCF\(^{β-TRCP}\) Suppresses Angiogenesis and Thyroid Cancer Cell Migration by Promoting Ubiquitination and Destruction of VEGF Receptor 2
    (The Rockefeller University Press, 2012) Shaik, Shavali; Nucera, Carmelo; Inuzuka, Hiroyuki; Gao, Daming; Garnaas, Maija; Frechette, Gregory Martin; Harris, Lauren; Wan, Lixin; Fukushima, Hidefumi; Husain, Amjad; Nose, Vania; Fadda, Guido; Sadow, Peter; Goessling, Wolfram; North, Trista; Lawler, Jack; Wei, Wenyi
    The incidence of human papillary thyroid cancer (PTC) is increasing and an aggressive subtype of this disease is resistant to treatment with vascular endothelial growth factor receptor 2 (VEGFR2) inhibitor. VEGFR2 promotes angiogenesis by triggering endothelial cell proliferation and migration. However, the molecular mechanisms governing VEGFR2 stability in vivo remain unknown. Additionally, whether VEGFR2 influences PTC cell migration is not clear. We show that the ubiquitin E3 ligase SCF\(^{β-TRCP}\) promotes ubiquitination and destruction of VEGFR2 in a casein kinase I (CKI)–dependent manner. β-TRCP knockdown or CKI inhibition causes accumulation of VEGFR2, resulting in increased activity of signaling pathways downstream of VEGFR2. β-TRCP–depleted endothelial cells exhibit enhanced migration and angiogenesis in vitro. Furthermore, β-TRCP knockdown increased angiogenesis and vessel branching in zebrafish. Importantly, we found an inverse correlation between β-TRCP protein levels and angiogenesis in PTC. We also show that β-TRCP inhibits cell migration and decreases sensitivity to the VEGFR2 inhibitor sorafenib in poorly differentiated PTC cells. These results provide a new biomarker that may aid a rational use of tyrosine kinase inhibitors to treat refractory PTC.