BRAF V600E Gene Mutation Is Associated With Bilateral Malignancy of Papillary Thyroid Cancer

Liu, Zhuo Ran; Lv, Tian; Xie, Cong; Di, Zhongmin

doi:10.1016/j.amjms.2018.04.012

Cited by 17 publications

(10 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, recurrence and metastasis are still the main causes of PTC treatment failure and death 7,8. There is increasing evidence that abnormal activation and dysfunction of key genes can lead to the progression of PTC 9,10. Therefore, investigation of molecular markers of PTC plays a crucial role in improving its therapeutic strategy and prognosis.…”

Section: Introductionmentioning

confidence: 99%

<p>MicroRNA-26a-5p inhibits proliferation, invasion and metastasis by repressing the expression of Wnt5a in papillary thyroid carcinoma</p>

Shi¹,

Wang²,

Ding³

et al. 2019

OTT

View full text Add to dashboard Cite

Background Thyroid cancer (TC) is considered as the fastest growing malignancy in the human endocrine system, particularly papillary thyroid cancer (PTC). MicroRNAs (miRs) serve as a role in promoting or suppressing tumors in various types of malignant tumor including PTC. This study aims to explore whether microRNA-26a-5p (miR-26a-5p) could affect the proliferation, invasion and metastasis ability of PTC cells by regulating Wnt5a. Materials and methods The expression of miR-26a-5p was examined by qRT-PCR in PTC tissue samples (58 cases, mean age 53 years old) and PTC cell lines (K1 and BCPAP). Cell proliferation, invasion and migration were tested with CCK8 assay, colony formation assay, transwell invasion assay and wound healing assay, respectively. Luciferase reporting experiment was used to verify that Wnt5a is a molecular target of miR-26a-5p. The relationship between miR-26a-5p and Wnt5a was analyzed by qRT-PCR and Western blot and was further proved by Pearson’s correlation analysis. Animal (24 nude mice) experiments were used to demonstrate that miR-26a-5p inhibits tumor growth by targeting Wnt5a. Results The expression of miR-26a-5p declined in PTC tissues ( P <0.01). The expression of miR-26a-5 was also significantly down-regulated in PTC tissues with advanced TNM stages ( P <0.01) and lymph node metastasis ( P <0.01) compared with normal thyroid tissues. Compared with normal human thyroid cell line Nthy-ori 3-1, the expression of miR-26a-5p in K1 cells and BCPAP cells were nearly 4.02-fold ( P <0.01) and 2.51-fold ( P <0.01) reduced. Up regulation of miR-26a-5p inhibited proliferation, colony formation, invasion and migration of PTC cells. MiR-26a-5p negatively regulated Wnt5a expression ( r =−0.887, P <0.01), yet Wnt5a overexpression reversed the tumor-suppressive effect of miR-26a-5p in PTC. Animal experiments further verified that miR-26a-5p inhibited PTC growth by targeting Wnt5a. Conclusion Overexpression of miR-26a-5p depresses proliferation, invasion, metastasis of PTC via Wnt5a. Therefore, miR-26a-5p may represent a potentially effective target gene for PTC.

show abstract

Section: Introductionmentioning

confidence: 99%

<p>MicroRNA-26a-5p inhibits proliferation, invasion and metastasis by repressing the expression of Wnt5a in papillary thyroid carcinoma</p>

Shi¹,

Wang²,

Ding³

et al. 2019

OTT

View full text Add to dashboard Cite

show abstract

“…[6,10,12,33] BRAF mutations are associated with a poor prognosis and tumor aggressiveness (extrathyroidal extension, lymph node metastasis, radioiodine treatment failure, and recurrence) and may be associated with the tumor being more often bilateral. [3,34] Without other coexisting genetic alterations, RAS mutated PTC lacks an aggressive behavior. [35] TERT promoter mutations correlate with aggressive clinicopathological features and poor outcomes.…”

Section: Discussionmentioning

confidence: 99%

Cytologic, histologic and molecular findings of papillary thyroid carcinoma variants, one institution’s experience

Falk

Ratnayaka

Sholl

et al. 2019

JST

View full text Add to dashboard Cite

Papillary thyroid carcinoma (PTC) has two major types, classic (PTCC) and follicular variant (FVPTC), which correlate with molecular findings and have varying clinical implications. We assessed the cytologic findings and subsequent surgical pathology findings with the molecular mutations in these two groups, including microcarcinomas. Fourty-four patients with PTC resections over a one-year period were retrospectively examined in conjunction with previous cytologic diagnoses. BRAF, NRAS and TERT promoter mutations for the resected specimens were analyzed. Correlation with previous cytology in regard to molecular mutations and tumor size (microcarcinoma) were made. Significantly more BRAF V600E mutations were seen with PTCC, whereas significantly more NRAS mutations were seen with FVPTC. TERT mutations were only seen with PTCC. Molecular studies for thyroid carcninomas are becoming increasingly more common and influence treatment and patient prognosis. BRAF and or TERT mutations are associated with a worse prognosis. NRAS mutations associated with FVPTC and may lead to milder cytologic changes compared to the BRAF- and TERT-driven PTCC.

show abstract

“…The BRAF V600E activating mutation is arguably the most well understood and studied genetic alteration in thyroid cancer. It is most common in PTC with a reported incidence of approximately 30-80% (70)(71)(72)(73)(74). BRAF mutations area also frequently seen in PDTC and ATC (approximately 40%) (75).…”

Section: Braf V600e Inhibitorsmentioning

confidence: 99%

Novel Therapeutics in Radioactive Iodine-Resistant Thyroid Cancer

2021

View full text Add to dashboard Cite

Iodine-resistant cancers account for the vast majority of thyroid related mortality and, until recently, there were limited therapeutic options. However, over the last decade our understanding of the molecular foundation of thyroid function and carcinogenesis has driven the development of many novel therapeutics. These include FDA approved tyrosine kinase inhibitors and small molecular inhibitors of VEGFR, BRAF, MEK, NTRK and RET, which collectively have significantly changed the prognostic outlook for this patient population. Some therapeutics can re-sensitize de-differentiated cancers to iodine, allowing for radioactive iodine treatment and improved disease control. Remarkably, there is now an FDA approved treatment for BRAF-mutated patients with anaplastic thyroid cancer, previously considered invariably and rapidly fatal. The treatment landscape for iodine-resistant thyroid cancer is changing rapidly with many new targets, therapeutics, clinical trials, and approved treatments. We provide an up-to-date review of novel therapeutic options in the treatment of iodine-resistant thyroid cancer.

show abstract

BRAF V600E Gene Mutation Is Associated With Bilateral Malignancy of Papillary Thyroid Cancer

Cited by 17 publications

References 17 publications

<p>MicroRNA-26a-5p inhibits proliferation, invasion and metastasis by repressing the expression of Wnt5a in papillary thyroid carcinoma</p>

<p>MicroRNA-26a-5p inhibits proliferation, invasion and metastasis by repressing the expression of Wnt5a in papillary thyroid carcinoma</p>

Cytologic, histologic and molecular findings of papillary thyroid carcinoma variants, one institution’s experience

Novel Therapeutics in Radioactive Iodine-Resistant Thyroid Cancer

Contact Info

Product

Resources

About