n breast cancer, and was associated with clinical characteristics and prognosis. Thus, UBA7 can be deemed as a potential biomarker in breast cancer, and may serve as a target in treatment. Copyright © Lin et al.MYB protooncogene-like 2 (MYBL2) is a transcription factor that is upregulated and significantly associated with various human cancer types. However, the potential role of MYBL2 in clear cell renal cell carcinoma (ccRCC) is yet to be elucidated. Therefore, the expression and biological functions of MYBL2 in ccRCC were assessed in the current study using The Cancer Genome Atlas (TCGA). A Wilcoxon signed-rank test was performed to compare MYBL2 expression between ccRCC and normal tissues. Moreover, the association between MYBL2 expression and various clinicopathological factors was estimated using both the Wilcoxon signed-rank test and logistic regression. The differences in prognosis between patients with high- and low-MYBL2 expression were analyzed via the Kaplan-Meier method and Cox regression analysis. Finally, gene set enrichment analysis (GSEA) was performed to investigate the biofunctions of MYBL2 in ccRCC. It was revealed that MYBL2 was upregulated in ccRCC, and that the MYBL2 high-expression phenotype was significantly associated with sex, a high histological grade, an advanced clinical stage, tumor stage, lymph node metastasis, distant metastasis and poor overall survival (OS). It was also revealed, via the Cox regression analysis, that the upregulation of MYBL2 expression was able to independently predict a poor prognosis in patients with ccRCC. GSEA indicated that the intestinal immune network for IgA production, primary immunodeficiency, the janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway, the cytosolic DNA-sensing pathway, the p53 signaling pathway and the chemokine signaling pathway were all enriched in the high-MYBL2 expression datasets. In conclusion, the present findings indicate that MYBL2 may be used as an independent prognostic factor in patients with ccRCC. Copyright © Sun et al.The most specific biomarker on the surface of regulatory T cells (Tregs) is the forkhead/wingeded-helix protein 3 (Foxp3). In contrast, the expression of interleukin-7 receptor (IL-7R) is low or negative in Tregs. The present study aimed to investigate the expression of Foxp3 and IL-7R in diffuse large B-cell lymphoma (DLBCL), and to analyse the clinicopathological characteristics of patients with DLBCL and their association with overall survival (OS). Immunohistochemistry was performed to detect the expression of Foxp3 and IL-7R on routinely processed formalin-fixed and paraffin-embedded specimens. The χ2 test was used to analyse the association between the expression of Foxp3 and IL-7R and the clinicopathological characteristics of patients with DLBCL. Survival curves were used to investigate the effect of Foxp3 and IL-7R on patient prognosis. The results demonstrated that high Foxp3 expression in tissue was associated with non- germinal centre B-cell (GCB)-type disease (P=0.012), International Prognostic Index score >0 (P=0.012), stage 3 or 4 tumour (P=0.045) and disease progression and stabilization period (P=0.032). In addition, IL-7R expression was associated with non-GCB-type disease (P=0.001) and extranodal lymphoma (P=0.008). Furthermore, expression of Foxp3 and IL-7R was not associated with OS (P=0.447 and P=0.201, respectively). Foxp3 and IL-7R expression in non-GCB-type lymphoma was significantly higher compared with that in GCB lymphoma.  https://www.selleckchem.com/products/Idarubicin.html  The expression of Foxp3 and IL-7R may therefore help the development of individualized treatment, prognostic prediction and therapy stratification. Copyright © Zhao et al.Transforming growth factor-β (TGFβ) is a secreted cytokine whose aberrant spatiotemporal expression is related to cancer progression and metastasis. While TGFβ acts as a tumor suppressor in normal and premalignant stages, TGFβ functions as a tumor promoter during the malignant phases of tumor progression by prompting cancer cells to undergo epithelial-mesenchymal transition (EMT), which enhances tumor cell invasion and ultimately promotes metastasis to other organs. Extensive studies have been performed to uncover the molecular and cellular mechanisms underlying TGFβ inducing EMT in cancer cells. Here, we suggested that ELK3, which encodes a protein that orchestrates invasion and metastasis of triple negative breast cancer cells, is a downstream target of TGFβ-SMAD3 in MDA-MB231 cells. ELK3 expression was increased in a time-dependent manner upon TGFβ treatment. Chemical and molecular inhibition of the TGFβ receptor blocked the ability of TGFβ to induce ELK3 expression. Small interfering RNA-mediated suppression analysis revealed that SMAD3 induces TGFβ signaling to express ELK3. Moreover, the results of the luciferase reporter assay and chromatin immunoprecipitation analysis showed that SMAD3 directly binds to the SMAD-binding element on the promoter of ELK3 to activate gene expression following TGFβ stimulation. We concluded that ELK3 is a novel downstream target of TGFβ-SMAD3 signaling in aggressive breast cancer cells. Copyright © Park et al.Immune checkpoint blockade (ICB) therapy is a treatment strategy for hepatocellular carcinoma (HCC); however, its clinical efficacy is limited to a select subset of patients. Next-generation sequencing has identified the value of tumor mutation burden (TMB) as a predictor for ICB efficacy in multiple types of tumor, including HCC. Specific driver gene mutations may be indicative of a high TMB (TMB-H) and analysis of such mutations may provide novel insights into the underlying mechanisms of TMB-H and potential therapeutic strategies. In the present study, a hybridization-capture method was used to target 1.45 Mb of the genomic sequence (coding sequence, 1 Mb), analyzing the somatic mutation landscape of 81 HCC tumor samples. Mutations in five genes were significantly associated with TMB-H, including mutations in tumor protein 53 (TP53), Catenin®1 (CTNNB1), AT-rich interactive domain-containing protein 1A (ARID1A), myeloid/lymphoid or mixed-lineage leukemia (MLL) and nuclear receptor co-repressor 1 (NCOR1). Further analysis using The Cancer Genome Atlas Liver Hepatocellular Carcinoma database showed that TP53, CTNNB1 and MLL mutations were positively correlated with TMB-H.