Anaplastic thyroid carcinoma: an epidemiologic, histologic, immunohistochemical, and molecular single-institution study

Deeken-Draisey, Audrey; Yang, Guang; Gao, Juehua; Alexiev, Borislav A.

doi:10.1016/j.humpath.2018.07.027

Cited by 72 publications

(72 citation statements)

References 32 publications

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“…Cytokeratin-19 (CK19), Hector Battifora mesothelial cell-1 (HBME-1) and galectin-3 are also frequently used in the diagnosis of PTC [29][30][31][32][33]. In PDTC and anaplastic thyroid cancer (ATC), expression levels of CK19 and HBME-1 may be altered or weakened whereas cyclin D1 expression is upregulated, compared to CPTC [34][35][36][37][38][39][40]. Kakudo et al reported that Ki67 labeling index >10% can be a predictor of aggressive thyroid tumors including PDTC [41].…”

Section: Immunohistochemical Profilesmentioning

confidence: 99%

Solid variant of papillary thyroid carcinoma: an under-recognized entity

Ohashi

2020

Endocr J

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Solid variant of papillary thyroid carcinoma (SVPTC) is a rare morphological variant of papillary thyroid carcinoma (PTC). SVPTC is histologically characterized by predominant solid, trabecular and insular nests of tumor cells while cytological features of PTC such as nuclear grooves and nuclear inclusions are preserved. In fine needle aspiration cytology smears, tumor cells of SVPTC may be presented in cohesive, syncytial or trabecular clusters accompanied by some discohesiveness in the absence of necrosis. Although SVPTC and poorly differentiated thyroid carcinoma (PDTC) share similar histological findings of solid nests, SVPTC can be differentiated from PDTC in the lack of tumor necrosis, severe nuclear atypia, and a higher mitotic index. Immunohistochemical expression of CK19 and HBME-1, common markers of PTC, is decreased in solid nests of SVPTC. In pediatric patients exposed to radiation after the Chernobyl nuclear accident, there was a higher prevalence of SVPTC with RET/PTC3 type rearrangement. BRAF mutations are also reported in a small number of adult patients with SVPTC without any prior radiation exposure. Patients with SVPTC may have a slightly higher incidence of metastasis and recurrence of the tumor compared to conventional PTC, although overall survival rate is comparable. In this article, the current knowledge of SVPTC will be reviewed and discussed with an emphasis on the histopathological feature.

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Section: Immunohistochemical Profilesmentioning

confidence: 99%

Solid variant of papillary thyroid carcinoma: an under-recognized entity

Ohashi

2020

Endocr J

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“…Promoter methylation of PTEN is also common in anaplastic thyroid cancer (ATC) [65]. PTEN methylation is related to gene changes of PI3K Akt pathway in thyroid tumors, including PTEN mutations, various subtypes of Ras mutations, PIK3CA mutations, and amplification [66,67]. One study analyzed 24 genetic alterations in the major genes of MAPK and PI3K-AKT pathways in 48 ATC samples and found that the majority of (81%) samples that harbored genetic alterations could be likely activated in both pathways [68].…”

Section: Dna Methylation In Atcmentioning

confidence: 99%

Research Progress of DNA Methylation in Thyroid Cancer

Zhu¹,

Xie²

2020

DNA Methylation Mechanism

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We have summarized increasing data from all kinds of experiment results of papers in recent years, which are associated with tumor suppressor genes, oncogenes, and thyroid-specific genes and attempt to elucidate the importance of epigenetic modifications and the mechanisms of aberrant DNA methylation in thyroid cancer in this review. The results showed that current articles have revealed the importance of epigenetic modifications and the different types of mechanisms in thyroid cancer. The mechanisms of DNA methylation related to thyroid cancer demonstrate that acquired epigenetic abnormalities together with genetic changes play an important role in alteration of gene expression patterns. Aberrant DNA methylation has been well known in the CpG regions. Among the genes identified, we have shown the status of DNA promoter methylation in papillary, follicular, medullary, and anaplastic thyroid cancer. It suggested that thyroid cancer subtypes present differential promoter methylation signatures, which will encourage potential thyroid cancer detection in its early stages, assessment of prognosis, and targeted cancer treatment.

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“…Despite rare, 14-39% of deaths related to thyroid carcinoma are attributable to ATC [2]. The incidence rate of ATC has increased from 1973 to 2014, and the mean length of follow-up was 14 months in USA [3,4]. ATC is characterized by the amass of several oncogenic alterations, and emerging evidence has suggested that the increase of oncogenic alterations contributes to the increased aggressiveness level [1].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA NEAT1 suppresses hypoxia-induced migration, invasion and glycolysis in anaplastic thyroid carcinoma cells through regulation of miR-206 and miR-599

et al. 2020

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Background: Anaplastic thyroid carcinoma (ATC) is one of the most aggressive and lethal malignancies. Long noncoding RNAs (lncRNAs) are being found to play crucial roles in ATC progression. Herein, we focused on the role of nuclear paraspeckle assembly transcript 1 (NEAT1) on ATC progression under hypoxia and underlying mechanisms governing it. Methods: The expression levels of NEAT1, miR-206 and miR-599 were assessed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell migration and invasion abilities were detected using transwell assays. Glucose consumption and lactate production were determined using a corresponding commercial assay kit. Western blot was performed to evaluate the level of hexokinase 2 (HK2). The targeted interplays between NEAT1 and miR-206 or miR-599 were confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Xenograft model was established to observe the effect of NEAT1 on tumor growth in vivo. Results: Our data indicated that NEAT1 was highly expressed in ATC tissues and cells, and hypoxia induced NEAT1 expression in ATC cells. NEAT1 depletion repressed ATC cell migration, invasion and glycolysis under hypoxia. Mechanistically, NEAT1 acted as a molecular sponge of miR-206 and miR-599. Moreover, the repressive effects of NEAT1 knockdown on ATC cell migration, invasion and glycolysis under hypoxia were mediated by miR-206 or miR-599. Additionally, NEAT1 knockdown weakened tumor growth in vivo. Conclusion: In conclusion, our study suggested that a low NEAT1 expression suppressed the migration, invasion, and glycolysis in ATC cells under hypoxia at least partially through modulating miR-206 and miR-599, providing new therapeutic strategies for ATC treatment.

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Anaplastic thyroid carcinoma: an epidemiologic, histologic, immunohistochemical, and molecular single-institution study

Cited by 72 publications

References 32 publications

Solid variant of papillary thyroid carcinoma: an under-recognized entity

Solid variant of papillary thyroid carcinoma: an under-recognized entity

Research Progress of DNA Methylation in Thyroid Cancer

Knockdown of lncRNA NEAT1 suppresses hypoxia-induced migration, invasion and glycolysis in anaplastic thyroid carcinoma cells through regulation of miR-206 and miR-599

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