Taken together, upregulated CELSR3 is an important regulator in the progression and prognosis of HCC. The hypomethylation of CELSR3 and its regulation in the cell cycle may be the potential molecular mechanism in HCC. © The author(s).Dysbindin has been reported to be correlated with several malignancies. However, the clinical significance and biological role of dysbindin in epithelial ovarian cancer remains largely unknown. Here we demonstrated that the mRNA and protein levels of dysbindin were significantly upregulated in EOC tissues compared with normal ovarian tissues. High levels of dysbindin were significantly correlated with worse clinicopathological characteristics and poor prognosis in EOC patients. Overexpression and silencing of dysbindin promoted and inhibited, respectively, invasion and metastasis of EOC cells in vitro and in vivo. Mechanistically, dysbindin activates phosphorylation of ERK to promote the epithelial-mesenchymal transition and to mediate the invasive and metastatic ability of EOC cells. Our findings suggest that dysbindin facilitates invasion and metastasis by promoting the EMT of EOC cells and may serve as a potential therapeutic target in EOC. © The author(s).Background African American women have not benefited equally from recently improved breast cancer survival. We investigated if this was true for all subsets. Methods We identified 395,170 patients with breast adenocarcinoma from the SEER database from 1990 to 2011 with designated race, age, stage, grade, ER and PR status, marital status and laterality, as control. We grouped patients into two time periods, 1990-2000 and 2001-2011, three age categories, under 40, 40-69 and ≥ 70 years and two stage categories, I-III and IV. We used the Kaplan-Meier and logrank tests to compare survival curves. We stratified data by patient- and tumor-associated variables to determine co-variation among confounding factors using the Pearson Chi-square test and Cox proportional hazards regression to determine hazard ratios (HR) to compare survival. Results Stage I-III patients of both races ≥ 70 years old, African American widowed patients and Caucasians with ER- and PR- tumors had worse improvements in survival in 2001-2011 than younger, married or hormone receptor positive patients, respectively. In contrast, African Americans with ER- (Cox HR 0.70 [95% CI 0.65-0.76]) and PR- (Cox HR 0.67 [95% CI 0.62-0.72]) had greater improvement in survival in 2001-2011 than Caucasians with ER- (Cox HR 0.81 [95% CI 0.78-0.84]) and PR- disease (Cox HR 0.75 [95% CI 0.73-0.78]). This was not associated with changes in distribution of tumor or patient attributes. Conclusions African American women with stage I-III ER- and PR- breast cancer had greater improvement in survival than Caucasians in 2001-2011. This is the first report of an improvement in racial disparities in survival from breast cancer in a subset of patients. © The author(s).Objectives Several factors associated with the prognosis of patients with NSCLC have been reported in the literature; however, most of these factors cannot be examined preoperatively. In this study, the clinical utility of platelet parameters in patients with NSCLC who underwent curative resection was evaluated. Materials and Methods A retrospective study on patients with NSCLC who underwent curative resection from July 2006 to September 2016 was conducted. The Cox proportional hazard regression model was applied to evaluate the variables that demonstrated effects on disease-free and overall survival (DFS and OS). Results A total of 116 patients with NSCLC were analyzed. There were 15 patients with plateletcrit greater than 0.2755%, and 101 patients whose plateletcrit was 0.2755% or lower. Multivariate analysis identified plateletcrit higher than 0.2755% (hazard ratio [HR] = 4.18, 95% confidence interval [CI] = 1.54-11.34, P =0.004), patient age of 65 years or more (HR = 4.02, 95% CI = 1.67-9.66, P = 0.001), and stage II or IIIA disease (HR = 2.95, 95% CI = 1.26-6.87, P = 0.012) as independent factors for OS that predicted a poor prognosis. Multivariate analysis identified plateletcrit higher than 0.2755% (HR = 4.07, 95% CI = 1.52-10.94, P = 0.005), stage II or IIIA disease (HR = 5.38, 95% CI = 2.71-10.66, P less then 0.001) and non-adenocarcinoma (HR = 1.92, 95% CI = 1.02-3.59, P = 0.040) as independent prognostic factors for DFS that predicted a poor prognosis. Conclusion Our results suggest a potential role of preoperative plateletcrit as an independent prognostic marker for patients with resectable NSCLC. © The author(s).Background Cervical cancer is one of the most common gynaecological malignancies. Emerging studies have documented that prolyl-4-hydroxylase α subunit 2 (P4HA2) is involved in multiple processes of cancer progression. However, the functional roles of P4HA2 in cervical cancer progression remain to be elucidated. Methods P4HA2 mRNA and protein levels were examined in cervical cancer tissues and cell line by qRT-PCR and western blot.  https://www.selleckchem.com/products/bi-3802.html  The correlation of the P4HA2 expression levels and prognosis of cervical cancer patients were analysed in TCGA cervical cancer cohort and tissue microarray (TMA) cohort. P4HA2 was silenced to evaluate its function on cervical cancer progression both in vitro and in vivo. Bioinformatics analysis was performed to investigate the underlying regulation mechanism of cervical cancer by P4HA2. Results We found that P4HA2 are markedly upregulated in cervical cancer tissues in comparison with adjacent non-neoplastic tissues. In addition, upregulation of P4HA2 was associated with shorter overall survival (OS) and relapse-free survival (RFS). Functionally, we demonstrated that P4HA2 knockdown attenuated cell proliferation, migration and invasion of cervical cancer cells. Furthermore, xenograft tumor mouse model experiment showed silencing P4HA2 significantly inhibited tumor growth in vivo. Mechanistically, bioinformatics analysis revealed that epithelial-mesenchymal transition (EMT) was involved in cervical cancer progression regulated by P4HA2 and we further confirmed knockdown P4HA2 suppressed the EMT process. Conclusion our results suggest that P4HA2 functions as an oncogene in promoting cervical cancer cell proliferation, migration and invasion by inducing EMT, which might be a promising prognostic factor and therapeutic target for cervical cancer. © The author(s).