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In recent years, immunotherapy has become a major research focus in the field of cancer treatment. Because of its good efficacy and lasting immune response, immune checkpoint inhibitors have benefited the long-term survival of many types of cancer patients. However, overactivation of the immune system may attack normal organs and cause a series of immune related adverse reactions. Among them, due to the high incidence of immune-related colitis, it deserves special attention. Camrelizumab is a programmed cell death 1 (PD-1) inhibitor that was developed by Jiangsu Hengrui Medicine Company. We reported the clinical data of a case of hepatocellular carcinoma with immune-related colitis after treatment with camrelizumab. A 63-year-old man with hepatocellular carcinoma developed diarrhea and hematochezia after receiving 4 cycles of camrelizumab. Endoscopy showed multiple flake congestion and edema in the terminal ileum and total colon mucosa with bright red surface. Pathological evaluation showed chronic inflammation of colonic mucosa. After giving 0.25g bid of enteric-coated sulfasalazine tablets orally for 6 weeks, his colitis improved. Camrelizumab can induce immune-related colitis. Sulfasalazine could be used to reduce adverse reactions of glucocorticoids. [ABSTRACT FROM AUTHOR]

aims to study the combinatory antitumor effect of apatinib and raltitrexed on human esophageal squamous carcinoma cells (ESCC). Materials and Methods: Two VEGFR-2-positive human ESCC lines, KYSE-30 and TE-1, were treated with apatinib or raltitrexed, or both, then the cell proliferation rate was measured by MTS assay; cell migration and invasion were studied by transwell assays; cell apoptosis rate was determined by flow cytometry; cellular autophagy level affected was analyzed by Western blot analysis; finally, quantitative polymerase chain reaction (qPCR) was used to monitor transcription and Western blot was performed to check phosphorylation of apoptotic proteins after treatment. Results: Both apatinib and raltitrexed significantly inhibited KYSE-30 and TE-1 cell proliferation in a dose-dependent manner. Treatment with both drugs showed enhanced inhibitory effects on cell proliferation, migration, and invasiveness compared with apatinib monotherapy. Apoptosis percentages in both cell lines were also remarkably increased by the combined treatment. Moreover, the combination of apatinib and raltitrexed down-regulated mRNA level of the anti-apoptotic protein Bcl-2, while up-regulated pro-apoptotic protein PARP, Bax, and caspase-3 transcription. Western blot analysis showed that phosphorylation levels of Erk, Akt, and invasiveness-associated protein matrix metalloproteinases-9 (MMP-9) were decreased in the combination group. Conclusion: Taken together, these results indicate that raltitrexed enhances the antitumor effects of apatinib on human ESCC cells by down-regulating phosphorylation of Akt and Erk, implying a combination of raltitrexed and apatinib might be an effective option for treating esophageal squamous cell carcinoma patients. [ABSTRACT FROM AUTHOR]

background and relatively low resolution of photos captured for the wound healing assay. For Figure 3A on page 2691, all Transwell images were captured and saved in one folder labelled by experimental date. Two overlapping images from different visual fields were captured from one well but labelled incorrectly and inadvertently selected for Figure 3A. The correct Figures 2 and 3 are shown in Download Article. The authors apologize for these errors and advise they do not affect the results of the paper. Read the original article [ABSTRACT FROM AUTHOR]

Background: Traditional chemotherapy and molecular targeted therapy have shown modest effects on the survival of patients with pancreatic cancer. The current study aimed to investigate the antitumor effects of apatinib, Astragalus polysaccharide (APS), and the combination of both the drugs in pancreatic cancer cells and further explore the molecular mechanisms in vitro. Materials and methods: Expression of vascular endothelial growth factor receptor-2 (VEGFR-2) in human pancreatic cancer cell lines ASPC-1, PANC-1, and SW1990 was detected by Western blotting. Cell proliferation was measured by MTS, and migration and invasion were detected by wound-healing and Transwell assays, respectively. Cell apoptosis rate was determined by flow cytometry and cellular autophagy level affected by apatinib, and APS was analyzed by Western blotting. Results: Human pancreatic cancer cell lines ASPC-1 and PANC-1 expressed VEGFR-2, but VEGFR-2 was not detected in SW1990. Either apatinib or APS inhibited cell proliferation in a dose-dependent manner in ASPC-1 and PANC-1. APS in combination with apatinib showed enhanced inhibitory effects on cell migration and invasion compared with apatinib monotherapy in ASPC-1 and PANC-1. Meanwhile, APS combined with apatinib strongly increased cell apoptosis percentage. Western blotting showed that the combination of APS and apatinib significantly enhanced the downregulation of phosphorylated protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) (p-AKT and p-ERK) as well as matrix metalloproteinases-9 (MMP-9) expression. In addition, both apatinib and APS induced cellular autophagy. However, the expression of autophagy-related proteins was not further elevated in the combination group. Conclusion: The study first demonstrated that apatinib showed potentially inhibitory effects in pancreatic cancer cells and that APS enhanced the antitumor effects of apatinib through further downregulating the expression of phosphorylation of AKT and ERK as well as MMP-9. [ABSTRACT FROM AUTHOR]