Tumor immune microenvironment (TIME) include tumor cells, immune cells, cytokines, etc. The interactions between these components, which are divided into anti-tumor and pro-tumor, determine the trend of anti-tumor immunity. Although the immune system can eliminate tumor through the cancer-immune cycle, tumors appear to eventually evade from immune surveillance by shaping an immunosuppressive microenvironment. Immunotherapy reshapes the TIME and restores the tumor killing ability of anti-tumor immune cells. Herein, we review the function of immune cells within the TIME and discuss the contribution of current mainstream immunotherapeutic approaches to remolding the TIME. Changes in the immune microenvironment in different forms under the intervention of immunotherapy can shed light on better combination treatment strategies.

Despite increasing evidence demonstrated robot-assisted distal gastrectomy (RADG) is safe and feasible for the treatment of advanced gastric cancer (AGC), robot-assisted total gastrectomy (RATG) remains a challenging procedure due to its technical difficulties and possible postoperative complications (POCs). This study aimed to systematically evaluate POCs following RATG. Between January 2017 and January 2019, 319 AGC patients with pathological stage T2-4aN0-3M0 who underwent RADG or RATG were enrolled. POCs were stratified using the Clavien-Dindo classification. One-to-one propensity score matching was performed to reduce confounding differences. After matching, 266 patients met the criteria for further analysis. Ultimately, 64 patients (24.1%) who developed POCs had 126 clinical manifestation events. Overall the POCs rate was significantly greater after RATG in comparison with RADG (29.3% vs. 18.8%; P = 0.045), and more major POCs (Clavien-Dindo grade ≥ IIIa) were observed in the RATG group (14.3% vs. 5.3%; P = 0.013). The POCs were then classified into local and systemic POCs. The rates of local POCs (35.3% vs. 19.5%; P = 0.004) and systemic POCs (24.8% vs. 15.0%; P = 0.046) were significantly higher in the RATG group than the RADG group. Subgroup analysis showed that the anastomotic leakage rate was higher after RATG (5.3% vs. 0.8%; P = 0.031), whereas the remaining POCs were similar between the two groups. Patients with higher POCs significantly had longer postoperative length of stay (R = 0.895, P = 0.003). Multivariate analysis confirmed age, extent of resection, and TNM stage were risk factors for all POCs. These findings demonstrated that RATG is technically feasible and safe for treatment of AGC with acceptable morbidity and mortality rates. The POCs rate of RATG was higher than RADG, especially for anastomotic leakage. More effective anastomotic techniques are needed in RATG to prevent leakage.

Pancreatic duct adenocarcinoma (PDAC) is an aggressive and lethal malignancy. Pancreatic cancer stem cells (PCSCs) are assumed to contribute to the initiation and invasion of PDAC. In this study, we performed single-cell RNA sequencing (scRNA-seq) analysis of PDAC tumor samples from patients and control pancreas tissues to reveal the transformation process of cancer stem cell (CSC)-like ductal cells into ductal cells with invasive potential and we screened out CSC-related genes (CRGs). Subsequently, we applied LASSO and Cox regression models to identify five CRGs with potential prognostic values and constructed a risk prognostic model using the Cancer Genome Atlas datasets. The risk models were verified using Gene Expression Omnibus datasets. Patients in the high-risk group had a significantly poor overall survival (Pvalue<0.0001), as illustrated by the Kaplan-Meier survival curve, and the area under the curve confirmed the accuracy of predictions by our risk model. Tumor mutation burden variations were used to further explore the differences between the two risk cohorts. In addition, the Human Protein Atlas was used to investigate the protein expression of five hub CRGs. In brief, we utilized scRNA-seq to reveal the invasive trajectory of ductal cells and identified crucial CRGs in PDAC, which may help predict patient survival and provide potential clinical therapeutic targets against CSCs. Graphical abstract

Objective. To evaluate Roux‐en‐Y and Billroth II reconstruction following pancreaticoduodenectomy (PD). Methods. PubMed, Embase, the Cochrane Library, and the Web of Science were searched to identify randomized controlled trials (RCTs) and controlled clinical trials that compared Roux‐en‐Y and Billroth II reconstruction following PD up to December 2019. RevMan 5.3 software was used for the statistical analysis. Results. Four RCTs and five controlled clinical trials were included, with a total of 1,072 patients (500 and 572 patients in the Roux‐en‐Y and Billroth II groups, respectively). No significant differences in delayed gastric emptying (DGE), A‐grade DGE, B‐grade DGE, or C‐grade DGE were observed between the Roux‐en‐Y and Billroth II reconstruction groups after PD (odds ratio [OR] = 1.01, 95% confidence interval [CI]: 0.50–2.03, P = 0.98; OR = 0.49, 95% CI: 0.17–1.45, P = 0.20; OR = 0.63, 95% CI: 0.29–1.38, P = 0.25; and OR = 2.13, 95% CI: 0.38–11.99, P = 0.39). No significant difference in the incidence of postoperative pancreatic fistula, abscess, bile leaks, infection, postoperative bleeding, or the length of the postoperative hospital stay was observed between the Roux‐en‐Y and Billroth II groups (P > 0.05), but the operation time was significantly different (mean difference [MD] = 31.65, 95% CI: 7.14–56.17, P = 0.01). Conclusions. Billroth II reconstruction after PD did not significantly reduce the incidence of DGE or other complications but shortened the operation time compared to Roux‐en‐Y reconstruction. However, the results must be verified by further high‐quality, large RCTs or controlled clinical trials.

Pancreatic cancer has a low survival rate globally. Anillin (ANLN) is involved in the pathogenesis of pancreatic cancer (PC). The present study used databases and reverse transcription‑quantitative PCR to investigate the association between ANLN expression, clinical variables and the survival rate of patients with pancreatic cancer. Gene expression of ANLN in normal and cancer tissues was analyzed using data from The Cancer Genome Atlas, Oncomine and Gene Expression database of Normal and Tumor tissues 2 and ANOVA, and the association between ANLN mRNA expression and ANLN genovariation was analyzed using cBioPortal. The association between ANLN expression and the survival, clinical, pathological and prognostic characteristics of PC was analyzed using Kaplan‑Meier (K‑M) survival analysis, Kruskal Wallis and Mann Whitney‑U tests, and logistic and Cox regression models. Gene Set Enrichment Analysis (GSEA) revealed the molecular pathways underpinning ANLN function in PC. Overexpression of ANLN was observed in PC cells (normal vs. tumor, P<0.01) and tissues (normal vs. tumor, P=0.008). Enhanced ANLN expression was associated with high tumor grade (grade 1 vs. grade 3, odds ratio: 5.662, P0.05). K‑M analysis suggested that increased ANLN expression was associated with poor survival (P=0.002). Univariate and multivariate analysis revealed the ANLN is an independent prognostic factor for PC (P<0.001). GSEA demonstrated the p53, cell cycle, DNA replication, mismatch repair, nucleotide excision repair and PC pathways were associated with low expression of ANLN. Overall, ANLN is more highly expressed in PC compared with in normal tissue, and is associated with poor differentiation. The expression of ANLN may be a novel prognostic marker of poor survival. Finally, ANLN exert its functions in PC through the p53, cell cycle, DNA replication, mismatch repair and nucleotide excision repair and pathways.