BYSL, which encodes the human bystin protein, is a sensitive marker for astrocyte proliferation during brain damage and inflammation. Previous studies have revealed that BYSL has important roles in embryo implantation and prostate cancer infiltration. However, the role and mechanism of BYSL in glioblastoma (GBM) cell migration and invasion remain unknown. We found that knockdown of BYSL inhibited cell migration and invasion, downregulated the expression of mesenchymal markers (e.g., β-catenin and N-cadherin), and upregulated the expression of epithelial marker E-cadherin in GBM cell lines. Overexpression of BYSL promoted GBM cell migration, invasion, and epithelial-mesenchymal transition (EMT).  https://www.selleckchem.com/products/incb28060.html  In addition, the role of BYSL in promoting EMT was further confirmed in a glioma stem cell line derived from a GBM patient. Mechanistically, overexpression of BYSL increased the phosphorylation of GSK-3β and the nuclear distribution of β-catenin. Inhibition of GSK-3β by 1-Azakenpaullone could partially reverse the effects of BYSL downregulation on the transcriptional activity of β-catenin, the expression of EMT markers, and GBM cell migration/invasion. Moreover, immunohistochemical analysis showed strong expression of BYSL in GBM tissues, which was positively correlated with markers of mesenchymal GBM. These results suggest that BYSL promotes GBM cell migration, invasion, and EMT through the GSK-3β/β-catenin signaling pathway.
  To assess the performance of deep neural network (DNN) and machine learning based radiomics on 3D computed tomography (CT) and clinical characteristics to predict benign or malignant sacral tumors.
 
  This single-center retrospective analysis included 459 patients with pathologically proven sacral tumors. After semi-automatic segmentation, 1,316 hand-crafted radiomics features of each patient were extracted. All models were built on training set (321 patients) and tested on validation set (138 patients). A DNN model and four machine learning classifiers (logistic regression [LR], random forest [RF], support vector machine [SVM] and k-nearest neighbor [KNN]) based on CT features and clinical characteristics were built, respectively. The area under the receiver operating characteristic curve (AUC) and accuracy (ACC) were used to evaluate different models.
 
  In total, 459 patients (255 males, 204 females; mean age of 42.1 ± 17.8 years, range 4-82 years) were enrolled in this study, including 206 cases of benign tumor and 253 cases of malignant tumor. The sex, age and tumor size had significant differences between the benign tumors and malignant tumors (
  = 10.854, 
  = -6.616, 
  = 2.843, 
  < 0.05). The radscore, sex, and age were important indicators for differentiating benign and malignant sacral tumors (odds ratio [OR]1 = 2.492, OR2 = 2.236, OR3 = 1.037, 
  < 0.01). Among the four clinical-radiomics models (RMs), clinical-LR had the best performance in the validation set (AUC = 0.84, ACC = 0.81). The clinical-DNN model also achieved a high performance (an AUC of 0.83 and an ACC of 0.76 in the validation set) in identifying benign and malignant sacral tumors.
 
  Both the clinical-LR and clinical-DNN models would have a high impact on assisting radiologists in their clinical diagnosis of sacral tumors.
 Both the clinical-LR and clinical-DNN models would have a high impact on assisting radiologists in their clinical diagnosis of sacral tumors.
  Myelodysplastic syndromes and acute leukemias after allogeneic stem cell transplantation (allo-SCT) are mainly caused by recurrence of the primitive leukemic clones. More rarely, they originate from donor hematopoietic stem cells, developing the so-called donor cell leukemia (DCL) or myelodysplastic syndromes (DC-MDSs). DCL and DC-MDS can be considered as an 
  model of leukemogenesis, and even if the pathogenetic mechanisms remain speculative, a genetic predisposition of donor progenitor cells, an altered host microenvironment, and the impairment of immune surveillance are considered the main causes.
 
  We report a case of DC-MDS diagnosed 5 years after an allo-SCT from a matched related donor (patient's sister) in a patient with Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia (Ph+ B-ALL). The sex-mismatch allowed us to identify the donor cell origin. At the onset, the DC-MDS was characterized by chromosome seven monosomy and 
  , 
  , and 
  mutations. Because of a familiar history of cof the posttransplant myelodysplasia and acute leukemias. The potential key role of the impaired immune surveillance and of long-lasting immunosuppression appears to be emerging in the development of this case of DC-MDS. Finally, this case reminds the importance to investigate the familiar genetic predisposition in donors with a familiar history of neoplasia.This study aims to investigate the antitumor effect and the possible mechanism of a microecological preparation (JK5G) in mice. The mice treated with AOM/DSS were then randomly divided into the two model groups and the JK5G group, and the blank control group was included. Fecal samples were used for liquid chromatography-mass spectrometry and 16S rRNA gene sequencing analyses to reveal metabolic perturbations and gut flora disorders to demonstrate the effects of JK5G. Compared with the mice in the control group, the weight and food intake of mice after JK5G treatment were both upregulated. Moreover, JK5G could inhibit the growth of colon tumors and prolong the survival rate of mice, as well as inhibit the levels of cytokines in serum. The proportions of lymphocytes, T cells, CD3+CD4+ T cells, and CD3+CD8+ T cells in the spleen of the JK5G mice were all significantly increased compared to those in the control group (p less then 0.05). Similarly, compared with the model group, the proportions of lymphocytes, ciated with the role of JK5G in improving the nutritional status of mice and regulating the tumor microenvironment by regulating the changes of intestinal microbiota and metabolite bands on different pathways.
  The receptor tyrosine kinase mesenchymal-epithelial transition factor (MET) is frequently altered in cancers and is a common therapeutic target for cancers with MET variants. However, abnormal MET alterations and their associations with patient outcome across different cancer types have not been studied simultaneously. In this study, we try to fill the vacancy in a comprehensive manner and capture the full MET alteration spectrum.
 
  A total of 10,967 tumor samples comprising 32 cancer types from The Cancer Genome Atlas (TCGA) datasets were analyzed for MET abnormal expression, mutations, and copy number variants (CNVs).
 
  MET abnormal expression, alteration frequency, mutation site distribution, and functional impact varied across different cancer types. Lung adenocarcinoma (LUAD) has most targetable mutations located in the juxtamembrane domain, and both high expression and amplification of MET are significantly associated with poor prognosis. Kidney renal papillary cell carcinoma (KIRP) harbored the third highest alteration frequency of MET, which was dominated by mutations.