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De-oxidizing and antiviral strength of Begonia medicinalis fractions.
Purpose Treatment protocols for occult central lymph node metastasis (LNM) associated with papillary thyroid cancer (PTC) located in the isthmus are debatable. We aimed to analyze the pattern of occult central LNM in isthmic PTC, including risk factors for bilateral paratracheal LNM. Patients and methods Consecutive patients with PTC were recruited to this study. All patients underwent total thyroidectomy and prophylactic bilateral central neck dissection. The clinicopathologic features and distribution of central LNM were compared between the two groups, and risk factors for bilateral paratracheal LNM were analyzed. Results A total of 174 patients with PTC were enrolled in this study, of whom 87 patients had isthmic PTC (study group) and 87 patients had lobe-originating PTC (control group). The two groups had comparable demographics and tumor features. There were higher frequencies of pretracheal LNM (P =0.001) and bilateral paratracheal LNM (P = 0.002) in the isthmic PTC group. Bilateral paratracheal LNM was significantly associated with age less then 55 years (P = 0.037), capsular invasion (P = 0.034), tumor location (isthmus) (P less then 0.001), BRAF gene mutation (P = 0.013), and pretracheal LNM (P less then 0.001). Isthmus location (odds ratio [OR] 4.116, 95% confidence interval [CI] 1.264-13.433, P = 0.019) and pretracheal LNM (OR 3.422, 95% CI 1.214-9.642, P = 0.020) were independent risk factors for bilateral paratracheal LNM. Conclusion Because of its unique anatomic location, isthmic PTC differs from PTC in the lobe with respect to pretracheal and bilateral paratracheal LNM, even in patients of comparable age, sex, tumor size, extrathyroidal extension, BRAF mutation, and pathologic TNM staging. The isthmus location was found to be an independent risk factor for bilateral paratracheal LNM. This information may contribute to the development of an appropriate surgical protocol for isthmic PTC.Purpose To develop and validate a PI-RADS-based nomogram for predicting the probability of clinically significant prostate cancer (csPCa) at initial prostate biopsy. Patients and methods From February 2015 to October 2018, 573 consecutive patients made up the development cohort (DC), and another 253 patients were included as an independent validation cohort (VC). Univariate and multivariate analysis were used for determining the dependent clinical risk factors for csPCa. Prediction model1 was constructed by integrating independent clinical risk factors. Then added the PI-RADS score to model1 to develop the prediction model2 and present it in the form of a nomogram. The performance of the nomogram was assessed by receiver operating characteristic curve, net reclassification improvement analysis, calibration curve, and decision curve. Results All clinical candidate factors were significantly different between csPCa and non-csPCa in both the DC and VC. Age, PSA density (PSAD), and free-to-total PSA ratio (f/t) were ultimately determined as dependent clinical risk factors for csPCa and integrated into prediction model1. Then, prediction model2 was developed and presented in a nomogram. In the DC, the nomogram (AUC=0.894) was superior to model1, PI-RADS score, or other clinical factors alone in detecting csPCa. Similar result (AUC=0.891) was obtained in the VC. NRI analysis showed that the nomogram improved the classification of patients significantly compared with model1. Furthermore, the nomogram showed favorable calibration and great clinical usefulness. Conclusion This study developed and validated a nomogram that integrates PI-RADS score with other independent clinical risk factors to facilitate prebiopsy individualized prediction in high-risk patients with csPCa.Introduction PLAC 2 is a tumor-suppressive lncRNA in glioma, while its roles in other types of cancer remain unclear. This study was carried out to explore the potential involvement of PLAC 2 in osteosarcoma (OS). Methods Expression levels of PLAC 2 in OS and paired non-tumor tissues from OS patients were determined by RT-qPCR. A follow-up study was performed to analyze the prognostic value of PLAC 2 for OS. Interactions between PLAC 2 and miR-93 were assessed by cell transfection, followed by RT-qPCR. Cell proliferation assay was performed to analyze cell proliferation. Results Our results showed that PLAC 2 was downregulated in OS tissues, and the high expression levels of PLAC 2 were associated with favorable overall survival of OS patients. MiR-93 was upregulated in OS tissues and its expression was inversely correlated with the expression of PLAC 2. In OS cells, overexpression of PLAC 2 resulted in downregulated miR-93, while overexpression of miR-93 did not affect the expression of PLAC 2. Overexpression of PLAC 2 led to decreased proliferation rate of OS cells, while overexpression of miR-93 showed opposite roles and reduced the overexpressing effects of PLAC 2. Conclusion PLAC 2 is downregulated in OS and regulates cancer cell proliferation through miR-93.Background Growing evidence directly suggested that circular RNAs (circRNAs) are crucial contributors in the course of cervical cancer (CC) onset and progression. Nevertheless, a large number of circRNAs have not been fully addressed in their function and underlying mechanisms during CC etiology. Purpose Our study focused on the function of circRNA MYLK (myosin light chain kinase), one novel tumor-related circRNA, in CC cell behaviors. Methods Firstly, we evaluated the expression profile of circMYLK in CC cells and in normal Ect1/E6E7 cell line. Moreover, the accurate function of circMYLK in CC cells was assessed via colony formation, CCK-8, EdU, and TUNEL assay. The association among circRNAs, miRNA, and target mRNAs was predicated by bioinformatics methods and validated in mechanical assays. Results We disclosed that circMYLK was up-regulated in CC cell lines and acted as a sponge of miR-1301-3p. Besides, downstream miR-1301-3p was capable of reversing circMYLK-mediated CC cell growth and apoptosis. Furthermore, we validated that circMYLK bound to miR-1301-3p as a sponge to upregulate RHEB (Ras homolog, mTORC1 binding) expression. OTS964 manufacturer As annotated in prior works, RHEB was responsible for mTOR signaling transduction. Therefore, we investigated whether circMYLK functioned its tumor-facilitating impact in CC through a RHEB-dependent mTOR signaling activation. Conclusion It was unveiled that circMYLK sponged miR-1301-3p to promote RHEB expression, which resulted in mTOR signaling activation and CC cell malignant growth.
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