Inhibition of medullary thyroid carcinoma cell proliferation and RET phosphorylation by tyrosine kinase inhibitors

Surgery ◽  
2002 ◽  
Vol 132 (6) ◽  
pp. 960-967 ◽  
Author(s):  
Mark S. Cohen ◽  
Hameda B. Hussain ◽  
Jeffrey F. Moley
Keyword(s):  
Cell Proliferation ◽  
Thyroid Carcinoma ◽  
Tyrosine Kinase ◽  
Medullary Thyroid Carcinoma ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Carcinoma Cell ◽  
Medullary Thyroid ◽  
Thyroid Carcinoma Cell

Re: “Inhibition of medullary thyroid carcinoma (MTC) cell proliferation and RET phosphorylation by tyrosine kinase inhibitors”

Surgery ◽  
2004 ◽  
Vol 135 (2) ◽  
pp. 241-242 ◽  
Author(s):  
Ivan Plaza Menacho ◽  
Jan Willem de Groot ◽  
Thera Links ◽  
John Plukker ◽  
Bart J.L. Eggen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Carcinoma ◽  
Tyrosine Kinase ◽  
Medullary Thyroid Carcinoma ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Medullary Thyroid

Search for Materials that Influence Human Medullary Thyroid Carcinoma Cell Proliferation

2009 ◽  
Vol 24 (2) ◽  
pp. 93 ◽  
Author(s):  
Hyun Won Shin ◽  
Hye Won Jang ◽  
Keun Sook Kim ◽  
Ji In Lee ◽  
Ji Young Park ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Carcinoma ◽  
Medullary Thyroid Carcinoma ◽  
Carcinoma Cell ◽  
Medullary Thyroid ◽  
Thyroid Carcinoma Cell

Update on the Treatment of Medullary Thyroid Carcinoma in Patients with Multiple Endocrine Neoplasia Type 2

2020 ◽  
Vol 52 (08) ◽  
pp. 588-597 ◽  
Author(s):  
Maran Ilanchezhian ◽  
Sophia Khan ◽  
Christian Okafor ◽  
John Glod ◽  
Jaydira Del Rivero
Keyword(s):  
Thyroid Carcinoma ◽  
Tyrosine Kinase ◽  
Medullary Thyroid Carcinoma ◽  
Tyrosine Kinase Inhibitors ◽  
Multiple Endocrine Neoplasia ◽  
Kinase Inhibitors ◽  
Multiple Endocrine Neoplasia Type ◽  
Medullary Thyroid ◽  
Endocrine Neoplasia ◽  
Endocrine Neoplasia Type

AbstractMedullary Thyroid Carcinoma (MTC) is a rare neuroendocrine cancer that accounts for 1–2% of thyroid cancers in the United States (U.S.). While most cases are sporadic, 25% of MTC cases are hereditary. These hereditary cases occur in the setting of Multiple Endocrine Neoplasia Type 2A (MEN2A) or 2B (MEN2B) driven by mutations in the Rearranged during Transfection RET proto-oncogene. This article discusses hereditary MTC in the setting of MEN2 and the treatment options available for it. The first line treatment for this disease is typically a total thyroidectomy and tyrosine kinase inhibitors. Two tyrosine kinase inhibitors, vandetanib and cabozantinib, have been approved for treatment of advanced MTC, but options beyond those are limited. However, several promising treatments are being studied, which are discussed in this review.

Therapeutic management of metastatic medullary thyroid carcinoma: Role of new tyrosine kinase inhibitors

2013 ◽  
Vol 60 (3) ◽  
pp. 152-153
Author(s):  
Antonia García-Martín ◽  
Pablo José López-Ibarra Lozano ◽  
Eva María Triviño-Ibáñez ◽  
Fernando Escobar-Jiménez
Keyword(s):  
Thyroid Carcinoma ◽  
Tyrosine Kinase ◽  
Medullary Thyroid Carcinoma ◽  
Tyrosine Kinase Inhibitors ◽  
Kinase Inhibitors ◽  
Therapeutic Management ◽  
Medullary Thyroid

scholarly journals Role of Complex Cyclin D1/Cdk4 in Somatostatin Subtype 2 Receptor-Mediated Inhibition of Cell Proliferation of a Medullary Thyroid Carcinoma Cell Line in Vitro

Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3530-3538 ◽  
Author(s):  
Federico Tagliati ◽  
Maria Chiara Zatelli ◽  
Arianna Bottoni ◽  
Daniela Piccin ◽  
Andrea Luchin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Thyroid Carcinoma ◽  
Cyclin D1 ◽  
Cell Line ◽  
Medullary Thyroid Carcinoma ◽  
Carcinoma Cell ◽  
Carcinoma Cell Line ◽  
Medullary Thyroid ◽  
Thyroid Carcinoma Cell

Somatostatin (SRIH) inhibits cell proliferation by interacting with five distinct SRIH receptor subtypes (SSTRs) activating several pathways in many tissues. We previously demonstrated that SRIH, by activating Src homology-2-containing protein, inhibits cell proliferation of the human medullary thyroid carcinoma cell line, TT, which expresses all SSTRs. However, the effects of SRIH on cell cycle proteins have not been investigated so far. We therefore evaluated the effects of SRIH and a selective SSTR2 agonist on cell cycle protein expression, mainly focusing on cyclin D1 and its associated kinases. Our data show that SRIH and the selective SSTR2 agonist, BIM-23120, reduce cell proliferation and DNA synthesis as well as induce a delay of the cell cycle in G2/M phase. Moreover, treatment with both SRIH and BIM-23120 decreases cyclin D1 levels, with a parallel increase in phosphocyclin D1 levels, suggesting protein degradation. Moreover, our data show an increase in glycogen synthase kinase-3β activity, which triggers phosphorylation-dependent cyclin D1 degradation. Indeed, we observed a reduction in cyclin D1 protein half-life under treatment with SRIH or the SSTR2 selective agonist. A reduction in cdk4 protein levels is also observed with a parallel reduction in Rb phosphorylation levels at Ser-780. Our data indicate that the subtype 2 receptor-mediated antiproliferative effect of SRIH on TT cell proliferation may be exerted through a decrease in cyclin D1 levels.

PKCδ plays an important in regulating human medullary thyroid carcinoma cell viability

2013 ◽  
Author(s):  
Daniela Mole ◽  
Erica Gentilin ◽  
Teresa Gagliano ◽  
Federico Tagliati ◽  
Maria Rosaria Ambrosio ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Cell Viability ◽  
Medullary Thyroid Carcinoma ◽  
Carcinoma Cell ◽  
Medullary Thyroid ◽  
Thyroid Carcinoma Cell

Cofilin is a mediator of RET-promoted medullary thyroid carcinoma cell migration, invasion and proliferation

2019 ◽  
Author(s):  
Elena Giardino ◽  
Rosa Catalano ◽  
Annamaria Barbieri ◽  
Donatella Treppiedi ◽  
Federica Mangili ◽  
...  
Keyword(s):  
Cell Migration ◽  
Thyroid Carcinoma ◽  
Medullary Thyroid Carcinoma ◽  
Carcinoma Cell ◽  
Medullary Thyroid ◽  
Thyroid Carcinoma Cell
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