Parathyroid carcinoma: Three case reports.

BACKGROUND: Parathyroid carcinoma (PC) is a rare, slow-growing malignant tumor and a rare cause of primary hyperfunctioning of the parathyroid, with a highly variable clinical course, depending on the aggressiveness of the individual tumor and the degree of hypercalcemia. CASE SUMMARY: The aim of this report is to summarize the diagnosis and treatment of three cases of PC and to review and conclude aspects regarding the three collected cases with reference to other relevant cases to explore the value of ultrasound in the diagnosis of PC. All three patients had hypercalcemia, consisting of a high serum calcium level and a high level of parathyroid hormone that was > 2-fold (even > 30-fold) of the normal upper limit. The ultrasonographic findings of the parathyroid gland showed that the glands were all > 30 mm, and the internal echo was uneven. All patients underwent surgery. PC in three cases was confirmed by routine histopathology and immunohistochemistry. CONCLUSION: As clinical signs and laboratory results are nonspecific, it is difficult to diagnose PC preoperatively, so imaging examinations are often needed.

Luteolin suppresses tumor progression through lncRNA BANCR and its downstream TSHR/CCND1 signaling in thyroid carcinoma.

The flavonoid luteolin is a natural antioxidant that usually occurs in its glycosylated form in many green vegetables, and has shown anticancer effects against various cancers. However, the potential tumor-suppressive role of luteolin in thyroid carcinoma and its underlying mechanism remain largely unknown. In current study, SBR assay, clone formation assay were employed to evaluate the effects of luteolin on thyroid cancer. We found that luteolin significantly inhibits thyroid cancer growth. The further mechanisms of its anticancer activity were analyzed by flow cytometry, quantitative real-time PCR, and Western blotting. We found that luteolin decreased the expression of BRAF-activated long noncoding RNA (BANCR), which further led to downregulation of TSHR and downstream oncogenic signaling. Moreover, overexpression of BANCR/TSHR signaling can largely abolish the anti-tumor effects of luteolin on thyroid carcinoma in vitro and in vivo. In conclusion, luteolin may serve as a potential important anticancer agent for thyroid carcinoma by blocking the BANCR/TSHR signaling.

Pin1 is related with clinical stage of papillary thyroid carcinoma.

BACKGROUND: The context and aim of this article was to investigate whether the expression level of Pin1 was in association with the clinical stage of papillary thyroid carcinomas. METHODS: Seventy-two patients who had been treated at the Affiliated Hospital of Qingdao University - Yantai YuHuangDing Hospital during January 2013 to December 2014 were rolled in. The expression levels of Pin1 using immunohistochemistry were tested and were divided into four groups according to the different clinical stages and final scores based on multiplying intensity and percentage value of IHC results. Data was analyzed with SPSS 20.0, and P value <0.05 had been chosen as significant. RESULTS: Considered from analysis result, the Pin1 expression status statistically significantly correlated with the PTC clinical stages (χ(2) = 8.128, P = 0.043); as the clinical stage proceeded, the intensity of Pin1 in PTC cells had been increased. But we did not find any relationships between immunohistochemical staining results and other clinicopathological characteristics. CONCLUSIONS: The PTC cells' intensity of Pin1 was in association with the clinical stage. The role played by Pin1 in PTC has been studied, and we need to further investigate the application of Pin1 in the treatment of PTC.

B-Raf mutation and papillary thyroid carcinoma patients.

Thyroid carcinoma is the most prevalent endocrine neoplasm globally. In the majority of thyroid carcinoma cases, a positive prognosis is predicted following administration of the appropriate treatment. A wide range of genetic alterations present in thyroid carcinoma exert their oncogenic actions partially through the activation of the mitogen-activated protein kinase pathway, with the B-Raf mutation in particular being focused on by experts for decades. The B-Raf gene has numerous mutations, however, V600E presents with the highest frequency. It is believed that the existence of the V600E mutation may demonstrate an association with the clinicopathological characteristics of patients, however, inconsistencies remain in the literature. A number of explanatory theories have been presented in order to resolve these discrepancies. Recently, it has been suggested that the V600E mutation may function as a target in a novel approach that may aid the diagnosis and prognosis of thyroid carcinoma, with a number of vying methods put forward to that effect. The current review aims to assist researchers in further understanding the possible association between B-Raf mutations and thyroid carcinoma.

BRAF-Activated Long Noncoding RNA Modulates Papillary Thyroid Carcinoma Cell Proliferation through Regulating Thyroid Stimulating Hormone Receptor.

PURPOSE: The importance of long noncoding RNAs (lncRNAs) in tumorigenesis has recently been demonstrated. However, the role of lncRNAs in development of thyroid cancer remains largely unknown. MATERIALS AND METHODS: Using quantitative reverse transcription polymerase chain reaction, expression of three lncRNAs, including BRAF-activated long noncoding RNA (BANCR), papillary thyroid cancer susceptibility candidate 3 (PTCSC3), and noncoding RNA associated with mitogen-activated protein kinase pathway and growth arrest (NAMA), was investigated in the current study. RESULTS: Of the three lncRNAs (BANCR, PTCSC3, and NAMA), expression of BANCR was significantly up-regulated while PTCSC3 and NAMA were significantly down-regulated in papillary thyroid carcinoma (PTC) compared to that in normal tissue. BANCR-knockdown in a PTC-derived cell line (IHH-4) resulted in significant suppression of thyroid stimulating hormone receptor (TSHR). BANCR-knockdown also led to inhibition of cell growth and cell cycle arrest at G0/G1 phase through down-regulation of cyclin D1. In addition, BANCR was enriched by polycomb enhancer of zeste homolog 2 (EZH2), and silencing BANCR led to decreased chromatin recruitment of EZH2, which resulted significantly reduced expression of TSHR. CONCLUSION: These findings indicate that BANCR may contribute to the tumorigenesis of PTC through regulation of cyclin D1 and TSHR.

Association between TCF7L2 polymorphisms and breast cancer susceptibility: a meta-analysis.

AIM: Our aim was to investigate the relationship between transcription factor 7-like 2 (TCF7L2) polymorphisms and breast cancer susceptibility. METHODS: PubMed, Embase and CNKI databases were used to search the related studies investigating the correlation between TCF7L2 polymorphisms and breast cancer susceptibility. Pooled ORs and 95% CIs, based on five genetic models, were applied to estimate the association betweenTCF7L2 polymorphisms and breast cancer. A fixed-effect model or a random-effect model was applied according to the between-study heterogeneity. RESULTS: We analyzed six single nucleotide polymorphisms (SNPs) in TCF7L2 gene, namely rs12255372, rs7903146, rs7900150, rs3750805, rs1225404 and rs7003146. The increased risk of breast cancer was associated with TCF7L2 polymorphisms (22 vs. 11: OR=1.16, 95% CI=1.02-1.32; 22+12 vs. 11: OR=1.06, 95% CI=1.02-1.10; 22 vs. 11+12: OR=1.15, 95% CI=1.04-1.27; 2 vs. 1: OR=1.07, 95% CI=1.02-1.13; 12 vs. 11: OR=1.05, 95% CI=1.01-1.09). Among the locus, rs7903146 polymorphism was significantly associated with the risk for breast cancer under five genetic models (TT vs. CC: OR=1.29, 95% CI=1.08-1.53; TT+CT vs. CC: OR=1.09, 95% CI=1.01-1.18; TT vs. CC+CT: OR=1.24, 95% CI=1.05-1.48; T vs. C: OR=1.11, 95% CI=1.04-1.19; CT vs. CC: OR=1.08, 95% CI=1.00-1.17). Additionally, rs7900150 also showed effects on the susceptibility of breast cancer (TT vs. AA: OR=1.22, 95% CI=1.07-1.39; TT+AT vs. AA: OR=1.06, 95% CI=1.00-1.14; TT vs. AA+AT: OR=1.21, 95% CI=1.07-1.37; T vs. A: OR=1.09, 95% CI=1.02-1.15; AT vs. AA: OR=1.04, 95% CI=1.01-1.33). Meanwhile, we found that rs3750805 polymorphism could increased the risk for breast cancer (TT+AT vs. AA: OR=1.12, 95% CI=1.01-1.24). CONCLUSION: Our meta-analysis demonstrates that TCF7L2 polymorphisms may increase the risk for breast cancer.