Epigenetic modifications in poorly differentiated and anaplastic thyroid cancer
Molecular and Cellular Endocrinology, ISSN: 0303-7207, Vol: 469, Page: 23-37
2018
- 44Citations
- 43Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations44
- Citation Indexes44
- 44
- CrossRef36
- Captures43
- Readers43
- 43
Review Description
Well-differentiated thyroid cancer accounts for the majority of endocrine malignancies and, in general, has an excellent prognosis. In contrast, the less common poorly differentiated thyroid carcinoma (PDTC) and anaplastic thyroid carcinoma (ATC) are two of the most aggressive human malignancies. Recently, there has been an increased focus on the epigenetic alterations underlying thyroid carcinogenesis, including those that drive PDTC and ATC. Dysregulated epigenetic candidates identified include the Aurora group, KMT2D, PTEN, RASSF1A, multiple non-coding RNAs (ncRNA), and the SWI/SNF chromatin-remodeling complex. A deeper understanding of the signaling pathways affected by epigenetic dysregulation may improve prognostic testing and support the advancement of thyroid-specific epigenetic therapies. This review outlines the current understanding of epigenetic alterations observed in PDTC and ATC and explores the potential for exploiting this understanding in developing novel therapeutic strategies.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0303720717302915; http://dx.doi.org/10.1016/j.mce.2017.05.022; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85020414433&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/28552796; https://linkinghub.elsevier.com/retrieve/pii/S0303720717302915; https://dx.doi.org/10.1016/j.mce.2017.05.022
Elsevier BV
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