Further studies indicated that upregulation of several antiapoptotic factors, downstream of EIF4E, was partially responsible for MCM3AP-AS1-induced chemoresistance. Moreover, miR-15a functioned as a link between MCM3AP-AS1 and EIF4E, and was sponged by MCM3AP-AS1. Finally, we showed that the MCM3AP-AS1/miR-15a/EIF4E axis regulated the chemoresistance of lymphoma cells in vitro and in vivo.
 
  MCM3AP-AS1/miR-15a/EIF4E axis plays a role in the chemoresistance of Burkitt lymphoma, and it might become a promising target for lymphoma therapeutics.
 MCM3AP-AS1/miR-15a/EIF4E axis plays a role in the chemoresistance of Burkitt lymphoma, and it might become a promising target for lymphoma therapeutics.
  Programmed death-ligand 1 (PD-L1) is a negative costimulatory molecule, and its main function is widely considered to be in the regulation of T cells. Tumor-associated macrophages (TAMs) are an important part of the tumor microenvironment, and they also play an important role in immunosuppression. However, the relationship between the expression of PD-L1 and TAMs in cervical carcinoma (CC) remains unclear. We detected the expression of PD-L1 and TAMs in tumor tissue to study the correlation between them.
 
  Immunohistochemical staining of PD-L1, CD68 (pan-macrophage), and CD163 (M2-like macrophage) was performed in 120 cases of cervical squamous cell carcinoma. Logistic regression analysis was used to evaluate the predictors related to positive PD-L1 expression. We also apply the Kaplan-Meier method to study the recurrence-free and overall survival rate of CC patients.
 
  The increase in PD-L1 expression in tumor cells (TC) was significantly correlated with the increase in CD163 density (
  =0.8550, 
  <0.00rophage infiltration can serve as a potential therapeutic target.Despite advances, patients with metastatic colorectal cancer (mCRC) still have poor long-term survival. Identification of molecular subtypes is important to guide therapy through standard treatment pathways and holds promise for the development of new treatments. Following standard first- and second-line chemotherapy plus targeted agents, many patients retain a reasonable performance status, and thus are seeking further effective treatment to extend life and maintain symptom control. The challenge lies in selecting the most appropriate therapy in the third- and fourth-line settings, from a range of options including the relatively new oral agents TAS-102 and regorafenib, or rechallenge with previous chemotherapy or anti-epidermal growth factor receptor (anti-EGFR) monoclonal antibodies (mAB). Beyond this, therapy consists of trials involving novel agents and new combinations of treatments with theoretical synergy and/or non-overlapping toxicity. There is a great focus on enhancing immunogenicity in mCRC, to reflect the impressive results of immunotherapy drugs in the small cohort with mismatch repair deficient (dMMR) mCRC. Rare molecular subtypes of mCRC are increasingly being identified, including Her2-positive disease, NTRK fusions and others. Clinical trials exploring the efficacy of immunomodulatory and precision agents are plentiful and will hopefully yield clinically meaningful results that can be rapidly translated into routine care.
  Central venous catheters (CVCs) have been demonstrated as a feasible method for chemotherapy delivery in colorectal cancer patients. The objective of our study was to explore the preference of colorectal cancer patients (89%) in our institution for port catheters (PCs) through comparing the costs and complications between peripherally inserted central venous catheters (PICCs) and PCs.
 
  Overall, 777 colorectal cancer patients (89%) were eligible for central venous catheter (CVC) insertions from January 1, 2017, to January 1, 2019. We retrospectively compared the costs and complications following the introduction of PICCs and PCs in the infusion of intravenous chemotherapy agents in patients with colorectal cancer.
 
  A total of 773 colorectal patients were enrolled. The total cost of PICC and PC was US $436.20 and US $976, respectively. The complication rate was higher in the PICC compared with the PC group (45% versus 4%, P <0.001). The late complication rate of the two groups was particularly pronounced (52% versus 7%, p < 0.001). The incidence rate of total complications, that were developed in patients, with and without hemostatic prophylaxis, was 0.7% versus 5.7% (p < 0.001).
 
  Port devices are associated with higher costs but fewer complications, compared to PICC in patients with colorectal cancer.
 Port devices are associated with higher costs but fewer complications, compared to PICC in patients with colorectal cancer.
  Metformin may exert the anticancer effect on multiple types of cancers and some potential mechanisms have been suggested. Our study was designed to determine the effect of metformin on the cell autophagy and autophagic flux via the AMPK-mTOR signaling pathway in human hepatocellular carcinoma (HCC) cells.
 
  MHCC97H and HepG2 cell lines were cultured and treated without and with metformin at various concentrations (2, 5, 10 and 20 mM) for 48 h. Then, 10 mM was determined as the optimal concentration and the HCC cells were treated with metformin for 12, 24, 48, and 72 h. MTT assay was used to assess the cell viability and Western blotting was used to determine the expression of proteins (LC3-II, p62, phospho-AMPKα, phospho-mTOR, mTOR, phospho-p70 S6 Kinase, p70 S6 Kinase, PARP1, Caspase-9 and Caspase-3). Autophagy inhibitor 3-methyladenine, EGFP-LC3 and mCherry-GFP-LC3B plasmid transfection were used for further study.
 
  Metformin inhibited significantly the viability of MHCC97H and HepG2 cells in a dose- and time-dependent manner. For the apoptotic properties, activation of Caspase-9 and Caspase-3 and PARP cleavage were not observed after treatment with metformin. MHCC97H cells were transfected with a EGFP-LC3 plasmid and treatment with metformin could lead to the increased level of LC3-II and decreased level of p62. In metformin-induced autophagy, AMPK expression was activated, and the phosphorylation levels of mTOR and p70 S6 Kinase were inhibited.  https://www.selleckchem.com/products/i-bet-762.html  Metformin treatment and mCherry-GFP-LC3B plasmid transfection showed that metformin could induce the autophagic flux. 3-Methyladenine (3-MA) partly abolished this effect.
 
  Metformin could induce the autophagy, autophagic flux, and activate the AMPK-mTOR signaling pathway in human HCC cells.
 Metformin could induce the autophagy, autophagic flux, and activate the AMPK-mTOR signaling pathway in human HCC cells.