DNA methylation alterations as therapeutic prospects in thyroid cancer

Zhang, K; Li, C; Liu, J; Tang, Xiaozhi; Li, Z

doi:10.1007/s40618-018-0922-0

Cited by 19 publications

(13 citation statements)

References 59 publications

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“…The aberrant DNA methylation of promoters and enhancers affects gene expression. Hypermethylation can lead to the silencing of tumor suppressor genes, leading to carcinogenesis; common examples in thyroid cancer include Ras association domain family 1; isoform A ( RASSF1A ); cyclin-dependent kinase inhibitor 2A ( CDKN2A or P16INK4A ); death-associated protein kinase1 ( DAPK ); tissue inhibitor of metalloproteinase-3 ( TIMP3 ); SLC5A8 ; SLC5A5 ; thyroid stimulating hormone receptor ( TSHR ); PTEN ; retinoic acid receptor β2 ( RARβ2 ); RAP1 GTPase activating protein (RAP1GAP); and fibroblast growth factor receptor (FGFR) 2 [ 73 , 74 , 75 , 76 ]. Targeted methylation analysis showed that PTC is more likely to exhibit hypomethylation than hypermethylation, compared with a normal thyroid; this is contrasted to FTC, which displays more hypermethylations than hypomethylations [ 76 , 77 ].…”

Section: Molecular Landscape Of Follicular Cell-derived Thyroid Cancermentioning

confidence: 99%

Emerging Biomarkers in Thyroid Practice and Research

Agarwal

Bychkov

Jung

2021

Cancers

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Thyroid cancer is the most common endocrine malignancy. Recent developments in molecular biological techniques have led to a better understanding of the pathogenesis and clinical behavior of thyroid neoplasms. This has culminated in the updating of thyroid tumor classification, including the re-categorization of existing and introduction of new entities. In this review, we discuss various molecular biomarkers possessing diagnostic, prognostic, predictive and therapeutic roles in thyroid cancer. A comprehensive account of epigenetic dysregulation, including DNA methylation, the function of various microRNAs and long non-coding RNAs, germline mutations determining familial occurrence of medullary and non-medullary thyroid carcinoma, and single nucleotide polymorphisms predisposed to thyroid tumorigenesis has been provided. In addition to novel immunohistochemical markers, including those for neuroendocrine differentiation, and next-generation immunohistochemistry (BRAF V600E, RAS, TRK, and ALK), the relevance of well-established markers, such as Ki-67, in current clinical practice has also been discussed. A tumor microenvironment (PD-L1, CD markers) and its influence in predicting responses to immunotherapy in thyroid cancer and the expanding arena of techniques, including liquid biopsy based on circulating nucleic acids and plasma-derived exosomes as a non-invasive technique for patient management, are also summarized.

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Section: Molecular Landscape Of Follicular Cell-derived Thyroid Cancermentioning

confidence: 99%

Emerging Biomarkers in Thyroid Practice and Research

Agarwal

Bychkov

Jung

2021

Cancers

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“…Frequent epigenetic silencing of the RASSF1A in thyroid carcinoma has been highlithed (109) alone or with NORE1A methylation and BRAF V600E mutations (110). RASSF1 methylation can be used as the therapeutic determinant in thyroid malignancies (111). In a meta-analysis it was reported as the most significant hyper-methylated region within thyroid carcinomas (112).…”

Section: Discussionmentioning

confidence: 99%

Promoter Methylation of Four Tumor Suppressor Genes in Human Papillary Thyroid Carcinoma

et al. 2019

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Background & Objective:Papillary thyroid cancer (PTC) is considered to be the most common type of thyroid malignancies. Epigenetic alteration, in which the chromatin conformation and gene expression change without changing the sequence of DNA, can occur in some tumor suppressor genes and oncogenes. Methylation is the most common type of epigenetic alterations that can be an excellent indicator of PTC invasive behavior.Methods:In this research, we determined the promoter methylation status of four tumor suppressor genes (SLC5A8, RASSF1, MGMT, and DNMT1) and compared the results of 55 PTC cases with 40 goiter patients. For methylation, we used the methylation-sensitive high resolution melting (MS-HRM) assay technique. The resulting graphs of each run were compared with those of 0%, 50%, and 100% methylated controls.Results:Our data showed that the promoter methylation of SLC5A8, Ras association domain family member 1(RASSF1), and MGMT were significantly different between PTC tissue and goiter with P-value less than 0.05. The most significant differences were observed in RASSF1; 77.2% of hyper-methylated PTC patients versus 15.6% hyper-methylated goiter samples (P<0.001). Conclusion:RASSF1 promoter methylation can be a PTC genetic marker. RASSF1 promoter methylation is under the impact of the methyltransferase genes (DNMT1 and MGMT), protein expression, and promoter methylation.

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“…The hypermethylation of DAPK leads to inactivation of the MAPK signalling pathway. Due to the important roles of PTEN and DAPK in early TC diagnosis, cancer screening, and treatment prospects, they are assigned the methylation status of a biomarker [ 68 , 103 ]. Different signaling pathways and BRAF inhibitors in thyroid cancer.…”

Section: Different Signalling Pathways and Braf Inhibitors In Tcmentioning

confidence: 99%

Epigenetic modification and BRAF gene mutation in thyroid carcinoma

et al. 2021

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Thyroid cancer remains the most prevailing endocrine malignancy, and a progressively increasing incidence rate has been observed in recent years, with 95% of thyroid cancer represented by differentiated thyroid carcinomas. The genetics and epigenetics of thyroid cancer are gradually increasing, and gene mutations and methylation changes play an important roles in its occurrence and development. Although the role of RAS and BRAF mutations in thyroid cancer have been partially clarified,but the pathogenesis and molecular mechanisms of thyroid cancer remain to be elucidated. Epigenetic modification refer to genetic modification that does not change the DNA sequence of a gene but causes heritable phenotypic changes in its expression. Epigenetic modification mainly includes four aspects: DNA methylation, chromatin remodelling, noncoding RNA regulation, and histone modification. This article reviews the importance of thyroid cancer epigenetic modification and BRAF gene mutation in the treatment of thyroid cancer.

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DNA methylation alterations as therapeutic prospects in thyroid cancer

Abstract: Based on what was discussed in this review, we suggest that integration of epigenetic and targeted therapies into conventional treatments will reduce the occurrence of refractory radioiodine differentiated thyroid cancer and improve the outcomes in aggressive thyroid cancer patients.

Cited by 19 publications

References 59 publications

Emerging Biomarkers in Thyroid Practice and Research

Emerging Biomarkers in Thyroid Practice and Research

Promoter Methylation of Four Tumor Suppressor Genes in Human Papillary Thyroid Carcinoma

Epigenetic modification and BRAF gene mutation in thyroid carcinoma

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