Objective:To explore the effect of LILRB2 on the proliferation and apoptosis of colorectal cancer SW480 cells, and to further explore its mechanism.Methods:Colorectal cancer SW480 cells were cultured in vitro and divided into blank control group, negative control group and experimental group. The expression of LILRB2 was detected by flow cytometry. The expression of LILRB2 was detected by qPCR, and the empty vector plasmid and the LILRB2 plasmid were transfected into SW480 cells respectively; cell proliferation was detected by CCK-8 method; cell apoptosis was detected by flow cytometry. Western blot was used to detect changes in the expression of related proteins.Results:The expression level of LILRB2 in SW480 was 0.84 ± 0.09, twice higher than that in FHC cells (0.38 ± 0.05) , and the difference was statistically significant ( P<0.05) . After virus infection, the expression of LILRB2 (0.48 ± 0.07) in SW480 cells of the experimental group decreased significantly. CCK-8 experiment results showed that after 12 hours of treatment, the proliferation of SW480 cells in the LILRB2 low expression experimental group was inhibited, and the percentage of apoptosis in SW480 cells in the LILRB2 low expression experimental group increased to 49.3%±1.2%, which was statistically significant ( P<0.05) compared with the percentage of apoptosis in the blank control group and the negative control group (7.48%±0.85%, 7.35%±0.93%) . The ROS level of SW480 cells in the experimental group with low LILRB2 expression was significantly higher than that in the blank control group and negative control group ( P<0.05) . After adding ROS scavenger NAC, the apoptosis of LILRB2 in the experimental group increased. Conclusion:The low expression of LILRB2 inhibits the proliferation of SW480 cells and induces apoptosis, which may play a role by regulating the level of ROS, providing a theoretical basis for the study of LILRB2 in colorectal cancer.

Objective: To investigate the clinicopathological features and molecular phenotypes of gastric cancer with enteroblastic dif-ferentiation (GCED). Methods: A retrospective analysis of 337 patients with gastric adenocarcinoma diagnosed by the pathology de-partment of the First Affiliated Hospital of Zhejiang University in March 2013-2017 was conducted. Of them, 8 patients were diag-nosed with gastric carcinoma with intestinal blastocyte differentiation. All the patients were elderly, including 6 men and 2 women. The onset age was 68-83 years (mean 76.6 years). Two cases had serum AFP≥200 μg/L before treatment. According to the histopatho-logical morphology, the immunophenotype was analyzed by immunohistochemistry, the SALL4 gene was detected using reverse tran-scription-polymerase chain reaction (RT-PCR), and the relevant literature was reviewed. Results: Microscopically, all cases had primi-tive enteroid structures, consisting of cubic or columnar cells with clear cytoplasm, and immunohistochemical staining showed positivi-ty for either AFP and GPC3 or SALL4. The expression of SALL4 mRNA was significantly increased by RT-PCR. Follow-up from 1 to 5 years showed that 5 patients had liver and other organ metastases, 2 patients died, and 1 patient survived without a tumor. Conclusions:GCED is a rare invasive gastric adenocarcinoma with a worse prognosis than that of normal intestinal adenocarcinoma. The treatment of general intestinal adenocarcinoma has little effect. There are some characteristic changes in histology. It would be helpful for diag-nosis and differential diagnosis if clinicians are familiar with the tumor spectrum and genetic characteristics. Target therapy for an origi-nal marker, such as SALL4, has a bright future.

Immune checkpoint inhibitors (ICIs) have been widely used in management of malignant tumor. Programmed death ligand 1 (PD-1)/programmed death ligand 1 (PD-L1) inhibitors have been introduced to treat non-small cell lung cancer (NSCLC) in recent years. Currently, PD-1/PD-L1 inhibitors are considered to have minor side effects and do not independently increase the risk of infection. However, they may cause immune-related adverse events (irAEs) that can require immunosuppressive therapy with corticosteroids and/or immunosuppressants, leading to opportunistic infections. Furthermore, there were reports about reactivation of chronic/latent infections without irAEs. Thus, immune checkpoint inhibitor related infections have drawn more and more attention in the world. In this paper, we described the potential mechanism, available clinical data and recommendation of diagnosis and management for PD-1/PD-L1 inhibitor related infections.