Notes

Curriculum Transition Via Lecture-Based to Team-Based Studying is a member of Enhanced Functionality on Internal Treatments In-Training Examination.
To explore whether the neutrophil-to-lymphocyte ratio (NLR) and its changes are related to tumor recurrence in grade II-IV glioma patients.

One hundred patients who underwent two surgeries (first for diagnosis and the second for recurrence) were retrospectively analyzed. Complete blood count was obtained preoperatively before any treatment. Basic NLR (before the first surgery) and NLR changes were calculated. Tumor recurrence was evaluated by progression-free survival (PFS) using the Kaplan-Meier method. Univariate and multivariate Cox regression analyses were used to determine the potential prognostic factors for PFS.

The PFS of patients with high basic NLR (≥4) (median 9 months) was shorter than that of patients with low basic NLR (<4) (median 23 months) (
= 0.004). Univariate and multivariate analyses both showed that basic NLR (before the first surgery) (≥4 vs <4) was an independent predictor of PFS (
= 0.011). Belumosudil manufacturer The PFS is also varied with NLR changes before two surgeries (
< 0.05). Thible method for clinical judgment of glioma recurrence but also provides a new idea for exploring the mechanism of glioma recurrence.
The effects of miR-139 on the tumorigenicity of triple negative breast cancer (TNBC) and the underlying mechanisms were investigated.

Normal human breast epithelial (MCF-10A) and TNBC cell lines (HCC1806 and BT549) were used for microRNA (miR)-139 overexpression, SOX8 overexpression, and knockdown studies as in vitro models of TNBC. The expression of SOX8 and miR-139 was detected by reverse transcription-polymerase chain reaction. CCK8 and clone formation assays were used to evaluate cell proliferation ability. Transwell assays and flow cytometry were used to test cell migration and apoptosis, respectively. Cell tumorigenicity was examined by tumor sphere formation assays. The interaction between miR-139 and SOX8 was examined by dual-luciferase reporter assays. The expression of SOX8, cleaved caspase-3, and cleaved caspase-9 was analyzed by Western blotting. The findings were validated in vivo using a nude mouse transplanted tumor model.

SOX8 expression was higher (P < 0.05) and miR-139 expression was lower (P < 0.05) in HCC1806 and BT549 cells than in MCF-10A cells. SOX8 overexpression significantly enhanced cell proliferation and migration, reduced the rate of cell apoptosis, and increased tumor sphere formation (P < 0.05) compared with the control group, whereas SOX8 knockdown had the opposite effect (P < 0.05). Overexpression of miR-139 markedly decreased cell proliferation and migration, increased cell apoptosis in vitro, and decreased tumor angiogenesis and volume in vivo (P < 0.05).

miR-139 suppressed the tumorigenicity of TNBC cells by targeting SOX8.
miR-139 suppressed the tumorigenicity of TNBC cells by targeting SOX8.
The serious side effect of current conventional treatments for patients with metastatic colorectal cancer (CRC) highlights the requirement of an alternative treatment strategy. Natural compounds, such as curcumin, have been gained much attention due to its low toxicity and anti-tumor effect.

qPCR and Western blot were used to measure the molecular changes induced by curcumin. Wound-healing assay and transwell assay were conducted to study the effect on cell migration and invasion. RT
PCR array was performed to identify the miRNAs involved in curcumin-repressed EMT. Three algorithms and luciferase reporter assay were used to identify EPM5 as a target of miR-200c. The bioinformatical analysis of TCGA-COAD and other CRC cohorts were used to examine the association of EPM5 with EMT signatures and clinical relevance. The ectopic expression or siRNA-mediated knockdown of
was applied to study the role of EPM5 in CRC.

Treatment with curcumin changed the epithelial-mesenchymal transition (EMT)-related gene expression, repressed cell migration and invasion in CRC cells. Its anti-tumor capability required the upregulation of miR-200c. EPM5 was a direct target of miR-200c and enriched in the consensus molecular subtype (CMS) 4 of CRC. Ectopic expression of EPM5 alone was sufficient to induce EMT in CRC. Downregulation of EPM5 was necessary for curcumin-repressed EMT, migration, and invasion. Higher expression of EPM5 was associated with the advanced TNM stages and poor survival in CRC.

Our data provide the first evidence that the curcumin inhibits EMT in CRC by upregulation of miR-200c and downregulation of EPM5, and the use of curcumin might be able to prevent or delay CRC progression.
Our data provide the first evidence that the curcumin inhibits EMT in CRC by upregulation of miR-200c and downregulation of EPM5, and the use of curcumin might be able to prevent or delay CRC progression.Recently, immunotherapies that target the interactions of programmed cell death 1 (PD-1) with its major ligands, programmed death ligand 1 (PD-L1) and programmed death ligand 2 (PD-L2), have achieved significant success. To date, several immune checkpoint inhibitors targeting the PD-1/PD-L1 pathway have been developed to treat melanoma, non-small cell lung cancer, head and neck cancer, renal cell carcinoma, and urothelial carcinoma. Despite promising outcomes with immunotherapy, there are many limitations to several current immune biomarkers for predicting immune benefits and to traditional imaging for evaluating the efficacy and prognosis of immunotherapy and monitoring adverse reactions. In this review, we recommend a novel imaging method, molecular imaging. This paper reviews the application and prospects of molecular imaging in the context of current immunotherapies in regard to the following aspects 1) detecting the expression of PD-1/PD-L1; 2) evaluating the efficacy of immunotherapy; 3) assessing patient prognosis with immunotherapy; 4) monitoring the toxicity of immunotherapy; and 5) other targets imaging.Triple-negative breast cancer (TNBC) is one of the most aggressive subtypes of breast cancer, accounting for approximately 15% of cases, and is defined by the lack of expression of hormone receptors (estrogen and progesterone receptors) and lack of amplification or overexpression of human epidermal growth receptor 2 (HER2). Due to the lack of targets of hormone receptors and HER2, treatment of TNBC or advanced TNBC relies on conventional chemotherapeutic agents, but their efficacy and prognosis are poor. In patients with advanced TNBC, poorer outcomes are observed. Recently, with the launch of clinical trials and advancements in molecular studies, targeted therapy for signaling transduction pathways, immunotherapy for immune checkpoints, and new chemotherapy strategies have provided feasible or potential therapeutic options for advanced TNBC. This review aimed to summarize recent progress in targeted therapy, immunotherapy, and chemotherapy for advanced TNBC.
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