2014
DOI: 10.1001/jamasurg.2014.1694
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Frequent Silencing of RASSF1A via Promoter Methylation in Follicular Thyroid Hyperplasia

Abstract: We demonstrate silencing of tumor suppressor RASSF1A in a subset of FTH in the absence of other known thyroid cancer-associated genetic and epigenetic changes. Silencing of RASSF1A and concurrent NF-κB activation demonstrate that a subset of FTH shares epigenetic changes and downstream signaling events associated with malignant lesions, suggesting that FTH may have the potential to be a premalignant lesion.

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Cited by 23 publications
(15 citation statements)
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“…Taking into account the rapid regrowth of the nodule where we found a follicular carcinoma ( Figure 1(b) ), it should be evaluated whether RFA might promote neoplastic cell transformation or the progression of undetected thyroid cancers. This is an important issue to address before recommending RFA for Thy3 nodules, since these nodules are considered premalignant precursors of follicular carcinoma [ 23 ], if they are not already a cytologically undetected thyroid cancer [ 19 ]. A few reports have already raised the issue of tumor regrowth in thyroid [ 24 ] as well as nonthyroid cancers [ 25 , 26 ].…”
Section: Discussionmentioning
confidence: 99%
“…Taking into account the rapid regrowth of the nodule where we found a follicular carcinoma ( Figure 1(b) ), it should be evaluated whether RFA might promote neoplastic cell transformation or the progression of undetected thyroid cancers. This is an important issue to address before recommending RFA for Thy3 nodules, since these nodules are considered premalignant precursors of follicular carcinoma [ 23 ], if they are not already a cytologically undetected thyroid cancer [ 19 ]. A few reports have already raised the issue of tumor regrowth in thyroid [ 24 ] as well as nonthyroid cancers [ 25 , 26 ].…”
Section: Discussionmentioning
confidence: 99%
“…Phosphorylation β loss of function in prostate cancer [119], CCL: overexpression inhibits cell proliferation and promote apoptosis in HepG2 cells [87] Mouse double KO: cholangiocarcinoma [46,101], HCC [120] Decreased mRNA level in tumour associated with node metastasis [121], mouse double KO: crypt dysplasia, colon adenoma [46,78,120] RASSF1, RASSF1A TSG: promoter hypermethylation and decrease expression in cancer: thyroid [122], oesophageal [123], prostate [124], colorectal, breast [125] TSG; promoter hypermethylation and decrease expression in CRC [126,127] SAV1, Salvador TSG: LOH and downregulation in renal cell carcinoma [128], no gene mutation in stomach, liver and lung cancer [129] CCL: overexpression induces apoptosis in MCF-7 cells [130] No gene mutation in CRC [129] LATS1 TSG: decrease expression in cancer: glioma [131], NSLC [132], sarcoma [133] and astrocytoma [134]. CCL: LATS1 degradation inhibits apoptosis in MCF10A cells [135] TSG: promoter hypermethylation and mRNA decrease in CRC [86] LATS2 TSG: decrease expression in: malignant mesothelioma (and LOH) [136], NSLC (no mutation found) [137] and astrocytoma [134] OG: overexpression in AML [138], nosopharyngeal carcinoma [139] TSG: downregulation in CRC [87] …”
Section: Stk4 Mst1 and Stk3 Mst2mentioning
confidence: 99%
“…Along with these genetic factors, epigenetic regulation plays a crucial role in the initiation and progression of various types of cancers 20. Epigenetic alterations, such as aberrant promoter methylation, can yield powerful biomarkers for early detection of diseases 21, 22, 23. A previous research of Belinsky et al24 displayed that aberrant methylation of the p16 might be involved in hepatocellular cancer, which might be a novel biomarker for early detection.…”
Section: Discussionmentioning
confidence: 99%