Ret Ptc
Mostrando 13-20 de 20 artigos, teses e dissertações.
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13. Tumorigênese Molecular Tiroideana: Implicações Para a Prática Médica
Esta revisão apresenta aspectos de utilidade prática da tumorigênese tiroideana. O mais importante é a possibilidade de se fazer o diagnóstico genético precoce dos indivíduos portadores de mutações do gene RET em famílias com carcinoma medular de tiróide e neoplasia endócrina múltipla tipo 2. Além disso, discutem-se dados relativos à patogêne
Arquivos Brasileiros de Endocrinologia & Metabologia. Publicado em: 2002-08
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14. Shc and Enigma Are Both Required for Mitogenic Signaling by Ret/ptc2
Ret/ptc2 is a constitutively active, oncogenic form of the c-Ret receptor tyrosine kinase. Like the other papillary thyroid carcinoma forms of Ret, Ret/ptc2 is activated through fusion of the Ret tyrosine kinase domain to the dimerization domain of another protein. Investigation of requirements for Ret/ptc2 mitogenic activity, using coexpression with dominan
American Society for Microbiology.
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15. The full oncogenic activity of Ret/ptc2 depends on tyrosine 539, a docking site for phospholipase Cgamma.
RET/PTC oncogenes, generated by chromosomal rearrangements in papillary thyroid carcinomas, are constitutively activated versions of proto-RET, a gene coding for a receptor-type tyrosine kinase (TK) whose ligand is still unknown. RET/PTCs encode fusion proteins in which proto-RET TK and C-terminal domains are fused to different donor genes. The respective Re
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16. Induction of a proinflammatory program in normal human thyrocytes by the RET/PTC1 oncogene
Rearrangements of the RET receptor tyrosine kinase gene generating RET/PTC oncogenes are specific to papillary thyroid carcinoma (PTC), the most frequent thyroid tumor. Here, we show that the RET/PTC1 oncogene, when exogenously expressed in primary normal human thyrocytes, induces the expression of a large set of genes involved in inflammation and tumor inva
National Academy of Sciences.
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17. Characterization of an inversion on the long arm of chromosome 10 juxtaposing D10S170 and RET and creating the oncogenic sequence RET/PTC.
RET/PTC is a transforming sequence created by the fusion of the tyrosine kinase domain of the RET protooncogene with the 5' end of the locus D10S170 designated by probe H4 and is frequently found activated in human papillary thyroid carcinomas. RET and D10S170 have been mapped to contiguous regions of the long arm of chromosome 10: q11.2 and q21, respectivel
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18. Ultraviolet Light Induces Redox Reaction–mediated Dimerization and Superactivation of Oncogenic Ret Tyrosine Kinases
The c-RET proto-oncogene encodes a receptor-type tyrosine kinase, and its mutations in the germ line are responsible for the inheritance of multiple endocrine neoplasia type 2A (MEN2A) and 2B (MEN2B). Ret kinases are constitutively activated as a result of MEN2A mutations (Ret-MEN2A) or MEN2B mutations (Ret-MEN2B). Here we demonstrate that UV light (UV) irra
The American Society for Cell Biology.
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19. Ret oncogene activation in human thyroid neoplasms is restricted to the papillary cancer subtype.
We have recently reported the activation of a new oncogene in human papillary thyroid carcinomas. This oncogene, papillary thyroid carcinoma (PTC), is a novel rearranged version of the ret tyrosine-kinase protooncogene. Thyroid neoplasms include a broad spectrum of malignant tumors, ranging from well-differentiated tumors to undifferentiated anaplastic carci
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20. Docking Protein FRS2 Links the Protein Tyrosine Kinase RET and Its Oncogenic Forms with the Mitogen-Activated Protein Kinase Signaling Cascade
The receptor tyrosine kinase RET functions as the signal transducing receptor for the GDNF (for “glial cell-derived neurotrophic factors”) family of ligands. Mutations in the RET gene were implicated in Hirschsprung disease (HSCR), multiple endocrine neoplasia type 2 (MEN 2), and thyroid carcinomas. In this report we demonstrate that the docking protein
American Society for Microbiology.