O-GlcNAcylation enhances anaplastic thyroid carcinoma malignancy

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O-GlcNAcylation enhances the invasion of thyroid anaplastic cancer cells partially by PI3K/Akt1 pathway

BACKGROUND The PI3K family participates in multiple signaling pathways to regulate cellular functions. PI3K/Akt signaling pathway plays an important role in tumorigenesis and development. O-GlcNAcylation, a posttranslational modification, is thought to modulate a wide range of biological processes, such as transcription, cell growth, signal transduction, and cell motility. O-GlcNAcylation is ca...

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Anaplastic Thyroid Carcinoma

Thyroid cancers represent about 1% of all human cancers. Differentiate thyroid carcinomas (DTCs), papillary and follicular cancers, are the most frequent forms, instead Anaplastic Thyroid Carcinoma (ATC) is estimated to comprise 1-2% of thyroid malignancies and it accounts for 14-39% of thyroid cancer deaths. The annual incidence of ATC is about one to two cases/million, with the overall incide...

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O-GlcNAcylation is increased in prostate cancer tissues and enhances malignancy of prostate cancer cells.

O-GlcNAc is an O-linked ?-N-acetylglucosamine moiety attached to the side-chain hydroxyl of a serine or threonine residue in numerous cytoplasmic and nuclear proteins. In this study, we detected the level of O-GlcNAc in prostate, liver and pancreatic cancer tissues, and found that the global O-GlcNAc modification also known as O-GlcNAcylation, is specifically increased in prostate cancer tissue...

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Anaplastic transformation of differentiated thyroid carcinoma.

Anaplastic thyroid cancer (ATC) is one of the most aggressive malignancies that arise from transformation of pre-existing differentiated thyroid cancer (DTC). However, the carcinogenic mechanism of anaplastic transformation remains unclear. We describe a case for huge goiter diagnosed as papillary thyroid carcinoma, which underwent thyroidectomy. The final histology showed anaplastic transforma...

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ژورنال

عنوان ژورنال: Oncology Letters

سال: 2016

ISSN: 1792-1074,1792-1082

DOI: 10.3892/ol.2016.4647