Wilsonlindholm1246

Three different comparisons were performed regarding the locations, which revealed that the specificity did not change regarding the locations while the sensitivity of Loc3 was higher than that of Loc1 and Loc2. Conclusions The preliminary data of 4.5-year single-center study proved that the isthmus location may be more beneficial to estimate the malignancy on the basis of toposonographic laterality of the nodules with undetermined cytology. This notewothy outcome may be considered particularly for the challenging cases with undetermined cytology in Endocrine Surgery and Thyroidology.Purpose Head and neck squamous cell carcinoma (HNSCC), arising from the squamous epithelium, is the most common head and neck cancer (HNC). Smoking and alcohol are well known risk factors for HNSCC, while some high-risk human papilloma virus (HPV) subtypes were specifically identified as a high-risk factors for developing oropharyngeal squamous cell carcinoma (OPSCC). In this study, we have conducted a systematic review and meta-analysis in order to investigate the possible synergistic role of smoking and HPV in the development of HNSCC. Methods We conducted a systematic search in two online databases PubMed and Cochrane Library, searching for studies published between 2010-2018. Sixteen studies met the inclusion criteria; a total of 2161 patients were included, comprising 1470 HPV-negative and 691 HPV-positive, respectively. Results The number of smokers between HPV-positive HNSCC patients (group A) and HPV-negative HNSCC patients (group B) was compared. We have found that smokers in HPV-positive group were statistically significantly less than smokers in HPV-negative group (OR=0.33 with 95% CI 0.18, 0.61). The test for overall effect was Z =3.61 (p=0.0003). Conclusion Smoking is less common in HPV positive group than in HPV negative group, and so probably smoking does not play a major role in the pathogenesis of HPV-positive HNSCC as in the pathogenesis of HPV-negative HNSCC.Purpose Nasopharyngeal carcinoma (NPC) is a highly invasive and metastatic cancer. The alterations of miRNA deregulation and pathway have been reported to be implicated in NPC progression. Here, we aimed to explore miR-204 role and mechanism in NPC development. Methods We examined the expression level of miR-204 in NPC tissues and NPC cells (HONE-1, 6-10B, HNE1) using reverse-transcription quantitative PCR (RT-qPCR) analysis. MTT, and transwell assays were used to analyze the effects of miR-204 on the proliferation, invasion and migration of NPC cells. Luciferase reporter gene assays were used to confirm the target gene of miR-204 in NPC cells. Results The results showed that miR-204 was downregulated, while CXCR4 was upregulated in NPC samples and cells with important functional consequences. Also, miR-204 expression was inversely correlated to CXCR4 expression and it was also associated with the clinicopathologic features. Ectopic expression of miR-204 was significantly suppressed, whereas downregulation of miR-204 facilitated the capacities of NPC cells proliferation, invasion and migration. Besides, it was also found that miR-204 mimic strongly decreased CXCR4 expression and miR-204 inhibitor increased CXCR4 expression. Furthermore, luciferase assay results demonstrated that CXCR4 was the direct target of miR-204. Conversely to miR-204 effect, knockdown of CXCR4 showed an inhibitory effect on NPC cell progression. Mechanistic investigations revealed that miR-204 regulated NF-κB signaling via CXCR4. Conclusion Taken together, our findings suggested that miR-204 regulated NPC progression by targeting CXCR4 through NF-κB signaling pathway.Purpose Glioma causes significant mortality worldwide. The currently available treatment strategies are flawed and the therapeutic targets are limited. Accumulating evidence suggests that microRNAs (miRs) are involved in the development and progression of different cancers. Herein, the therapeutic potential of miR-9 was explored in human glioma cells. Methods The qRT-PCR was used for expression analysis. WST-1 assay was used for determination of cell viability. Acridine orange (AO) / ethidium promide (EB) and annexin V/propidium iodide (PI) were used for the detection of apoptosis. Flow cytometry was used for cell cycle analysis. Wound healing and transwell assays were used to monitor cell migration and invasion. Protein expression was determined by western blot analysis. Results The results showed that miR-9 is significantly downregulated in glioma cells. Overexpression of miR-9 caused significant inhibition in the proliferation of U87 glioma cells. The miR-9-triggered growth inhibition was mainly due to the induction of apoptosis which was concomitant with increase in the Bax/Bcl-2 ratio. Overexpression of miR-9 also induced arrest of U87 glioma cells at G2/M checkpoint of cell cycle. Additionally, transwell and wound healing assays showed that miR-9 caused significant decrease in the migration and invasion of U87 glioma cells. Bioinformatics analysis showed that miR-9 exerts its effects by inhibiting Cadherin-1 (CDH1). https://www.selleckchem.com/products/picropodophyllin-ppp.html However, overexpression of CDH1 could nullify the effects of miR-9 on the growth, migration and invasion of glioma cells. Conclusion Taken together, miR-9 may exhibit therapeutic implications in the treatment of glioma.Purpose Despite the emergence of innovative cancer treatment strategies, the global burden imposed by malignant glioma is expected to increase. Therefore there is an immediate need to find novel and better approaches for its treatment. The main aim of the current research work was to evaluate the anticancer effects of naturally occurring catechin flavonoid along with examining its effects on cell autophagy, cell cycle phase distribution, cell migration and invasion and MAPK/ERK signalling pathway. Methods MTT cell viability assay was used to assess the effects on cell proliferation and clonogenic assay was used to assess the effects on cell colony formation. Transmission electron microscopy (TEM) and western blot assay were used to examine the effects on autophagy. Flow cytometry was used to assess the effects of catechin on cell cycle, while the effects on cell migration and cell invasion were examined by wound healing assay and transwell chambers assay. Effects on MAPK/ERK signalling pathway were assessed by western blot assay.