Notes

Animal- vs . throughout vitro-derived antibodies: steering clear of the extreme conditions.
Immune checkpoint inhibitors such as programmed death protein 1/programmed death-ligand 1 and cytotoxic T-lymphocyte-associated protein 4 inhibitors are already playing a central role in the treatment of metastatic renal cell carcinoma. However, they seem to be only effective in a subset of patients, with a high risk of innate and adaptive tumor resistance. Consequently, biomarkers capable of predicting immune treatment efficacy in advanced renal cancer are needed both in the clinical and the experimental setting. We hereby present a brief summary of evidence on the most studied biomarkers in metastatic renal cell carcinoma with a focus on the possible future place of T cell immunoglobulin and mucin domain-3 (TIM-3).
Carrimycin is a newly synthesized macrolide antibiotic with good antibacterial effect. Exploratory experiments found its function in regulating cell physiology, proliferation and immunity, suggesting its potential anti-tumor capacity. The aim of this study is to investigate the anti-tumor effect of carrimycin against human oral squamous cell carcinoma cells in vitro and in vivo.

Human oral squamous cell carcinoma cells (HN30/HN6/Cal27/HB96 cell lines) were treated with gradient concentration of carrimycin. Cell proliferation, colony formation and migration ability were analyzed. LNG-451 Cell cycle and apoptosis were assessed by flow cytometry. The effect of carrimycin on OSCC in vivo was investigated in tumor xenograft models. Immunohistochemistry, western blot assay and TUNEL assays of tissue samples from xenografts were performed. The key proteins in PI3K/AKT/mTOR pathway and MAPK pathway were examined by western blot.

As the concentration of carrimycin increased, the proliferation, colony formation and migration ability of OSCC cells were inhibited. After treating with carrimycin, cell cycle was arrested in G0/G1 phase and cell apoptosis was promoted. The tumor growth of xenografts was significantly suppressed. Furthermore, the expression of p-PI3K, p-AKT, p-mTOR, p-S6K, p-4EBP1, p-ERK and p-p38 were down-regulated in vitro and in vivo.

Carrimycin can inhibit the biological activities of OSCC cells in vitro and in vivo, and regulate the PI3K/AKT/mTOR and MAPK pathways.
Carrimycin can inhibit the biological activities of OSCC cells in vitro and in vivo, and regulate the PI3K/AKT/mTOR and MAPK pathways.
Circulating tumor DNA (ctDNA) has been investigated as a potential prognostic biomarker to evaluate the therapeutic efficacy and disease progression in melanoma patients, yet results remain inconclusive. The purpose of this study was to illustrate the prognostic value of ctDNA in melanoma.

To describe the clinical prognostic value of ctDNA for melanoma patients.

Searched for eligible articles from Pubmed, Web of Science and Embase.Pooled hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated to evaluate the association between ctDNAat baseline or during treatmentand overall survival (OS) and progression-free survival (PFS).

A total of 9 articles were obtained, involving 617 melanoma patients. The pooled HRs revealed that compared with baseline undetectable ctDNA patients, detectable ctDNA was highly correlated with poor OS (HR 2.91, 95% CI 2.22-3.82;p< 0.001) and PFS (HR 2.75, 95% CI 1.98-3.83;p< 0.001). A meta-analysis of these adjusted HRs was performed and confirmed that ctDNA collected at baseline was associated with poorer OS/PFS (OS HR 3.00, 95% CI 2.19-4.11,p< 0.001/PFS HR 2.68, 95% CI 1.77-4.06,p< 0.001). During treatment, a significant association was shown between ctDNA and poorer OS/PFS (OS HR 6.26, 95% CI 2.48-15.80,p< 0.001; PFS HR 4.93, 95% CI 2.36-10.33,p< 0.001).

Investigation and application of ctDNA will improve "liquid biopsy" and play a role in early prediction, monitoring disease progression and precise adjusting treatment strategies in melanoma patients.
Investigation and application of ctDNA will improve "liquid biopsy" and play a role in early prediction, monitoring disease progression and precise adjusting treatment strategies in melanoma patients.
Endoscopic retrograde cholangiopancreatography (ERCP) may be inappropriate for most patients with choledocholithiasis. This study aimed to evaluate one-step percutaneous transhepatic cholangioscopic lithotripsy (PTCSL) in the treatment of patients with choledocholithiasis who could not undergo ERCP (e.g., failed ERCP, altered anatomy, and/or contra-indications).

This was a retrospective single-centre series of 67 patients who underwent choledocholithiasis between November 2015 and March 2018 35 with one-step PTCSL (Group A) and 32 with laparoscopic common bile duct (CBD) exploration (Group B).

Compared with Group B, Group A showed shorter duration of operation, length of stay in the hospital, postoperative hospital stay, postoperative drainage time, and time to oral intake (all P<0.05). Intraoperative blood loss, costs, conversion to open surgery (one in group A vs. seven in group B; P=0.023), and bile leakage (none in group A vs. four in group B; P=0.047) were lower in Group A than in Group B. There were no significant differences between the two groups regarding the intraoperative clearance rate, ultimate clearance rate, and several postoperative complications.

One-step PTCSL could be an alternative for patients with choledocholithiasis, especially when ERCP is not feasible.
One-step PTCSL could be an alternative for patients with choledocholithiasis, especially when ERCP is not feasible.
Long non-coding RNAs (LncRNAs) are broadly transcribed in the genome of human and animals, they play critical roles in cellular process, and participate in the progression of multiple diseases, including cancer. SLC16A1-AS1 is a tumor suppressive lncRNA in lung cancer. This study aimed to investigate the involvement of lncRNA SLC16A1-AS1 in hepatocellular carcinoma (HCC).

A total of 64 HCC patients were subjected to biopsy to obtain paired HCC and non-tumor tissues. Expression of SLC16A1-AS1 and miR-141 in paired tissues was determined by RT-qPCR. Correlations were analyzed by linear regression. Overexpression of SLC16A1-AS1 and miR-141 were achieved in HCC cells to explore the interactions between them. The methylation of the gene encoding miR-141 in HCC cells was detected by methylation-specific PCR (MSP). CCK-8 assay was performed for cell proliferation assay.

SLC16A1-AS1 was upregulated in HCC and its high expression levels predicted poor survival of HCC patients. Expression levels of miR-141 were lower in HCC patients and were inversely correlated with the expression levels of SLC16A1-AS1.
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