In the tumour microenvironment (TME), immunogenic cell death (ICD) plays a major role in stimulating the dysfunctional antitumour immune system. Chronic exposure of damage‐associated molecular patterns (DAMPs) attracts receptors and ligands on dendritic cells (DCs) and activates immature DCs to transition to a mature phenotype, which promotes the processing of phagocytic cargo in DCs and accelerates the engulfment of antigenic components by DCs. Consequently, via antigen presentation, DCs stimulate specific T cell responses that kill more cancer cells. The induction of ICD eventually results in long‐lasting protective antitumour immunity. Through the exploration of ICD inducers, recent studies have shown that there are many novel modalities with the ability to induce immunogenic cancer cell death. In this review, we mainly discussed and summarized the emerging methods for inducing immunogenic cancer cell death. Concepts and molecular mechanisms relevant to antitumour effects of ICD are also briefly discussed.

Abstract. Diabetes mellitus (DM) complications affect patients and cause varying damage. Skin ulcers exhibit difficulties in wound healing, and the regulatory basis for this remains unclear. High glucose concentration (HG) was utilized to mimic DM in cultured cells. Reverse transcription-quantitative polymerase chain reaction, western blotting and fluorescence dye analyses were performed to analyze the effects of hedgehog signaling in regulation of HG or diabetes in fibroblasts. HG-stress suppressed hedgehog-signaling gene expression, whereas the apoptosis and inflammatory response markers, Caspase-3 and plasminogen activator inhibitor-1 (PAI1), respectively, were induced. In addition, HG-stress inhibited the fibroblast proliferation rate. In parallel, treatment with Sonic hedgehog (Shh), an activator of hedgehog signaling, together with HG eliminated effects of HG on expression of hedgehog-signaling genes, Caspase-3 and PAI1, and rescued the cell proliferation rate in fibroblasts. In addition, Shh application activated c-Jun N-terminal kinase (JNK), which was inhibited by HG stress. sp600125, a JNK specific inhibitor, treatment inhibited the effect of Shh on fibroblast proliferation and hedgehog-signaling marker gene expression. Furthermore, zinc finger protein Gli1 (Gli1) overexpression partially eliminated the effect of HG and sp600125 on fibroblast proliferation, and reduced HG-induced ROS generation in fibroblasts. Together, these results indicate that HG stress inhibits hedgehog signaling, and Shh-JNK-Gli1 pathway positively regulates HG-induced damage on fibroblasts.

Background Hepatocellular carcinoma (HCC) patients often undergo curative liver resection to treat this form of cancer. Hepatectomy is, however, a form of major surgery associated with many significant risks including prolonged hospitalization, high costs, impaired physiological function, and high postoperative complication rates. Enhanced recovery after surgery (ERAS) is a multidisciplinary approach that seeks to expedite postoperative recovery in patients undergoing major surgeries in order to lower postoperative complication rates. This study was thus designed to assess the efficacy and safety of individualized ERAS approaches in patients undergoing hepatectomy.  Methods In total, we retrospectively analyzed data from 90 HCC patients that underwent hepatectomy between October 2018 and August 2019. All patients met the study enrollment criteria and provided written informed consent to participate. All studies were approved by the Hospital Research Ethics Committee and were consistent with the Declaration of Helsinki. Patients were randomly divided into two groups (n = 45 each) based on the employed perioperative treatment strategies: a conventional treatment group and an ERAS treatment group. Key outcomes were then compared between groups, including postoperative pain scores, duration of postoperative hospitalization, medical costs, and rates of readmission.  Results ERAS treatment was associated with lower postoperative pain scores at 24, 48, and 72 h post-treatment (P < 0.05), with a shorter postoperative hospitalization duration (8.16 days vs.10.49 days; P < 0.004), and with lower medical costs (P < 0.004) as compared to traditional treatment. No significant differences in complication rates (P > 0.05) or readmission rates (P > 0.557) were observed between these groups.  Conclusions Individualized ERAS improves patient postoperative recovery more effectively than traditional treatment in patients undergoing hepatectomy.