As an important metal element in human body, copper can be involved in many important biological processes such as cell metabolism, anti-oxidation, detoxification, iron absorption and so on. Copper in the human body is mainly ingested through diet, combined with transport proteins in the digestive tract into the blood, and then transported to all tissues of the body through carrier proteins. It is strictly regulated by copper ion chaperone protein and carrier protein, and its intake and excretion are in a dynamic balance. Copper plays an important role in tumor cell growth, migration and angiogenesis, so when copper homeostasis is out of balance, it can affect tumor cell growth and lead to apoptosis. Recent studies have found that copper can induce a new type of cell death - Cuprotosis, which is different from the classical cell death forms such as necrosis, pyrodeath, autophagy and necrotic apoptosis, and is closely related to the regulation of copper metabolism. Therefore, the novel cell death mechanism induced by copper has triggered extensive research. In the breast cancer related research, it was found that the genes and proteins related to copper death play an important role in the progression of breast cancer disease, immune cell infiltration, drug resistance, combination therapy and disease prognosis assessment, etc. Therefore, the cuprotosis mechanism should be further studied and applied in clinical anti-tumor therapy. It is expected to provide new treatment options for breast cancer patients.

Pancreatic cancer is one of the common gastrointestinal malignancies, the incidence of which is increasing year by year and has become one of the most important public health problems worldwide. At present, tumor treatment has entered the era of immunotherapy, but the response of pancreatic cancer patients to immune checkpoint inhibitors is not ideal. In addition, there is a lack of effective and validated biomarkers to stratify patients who may benefit from immunotherapy. This review has summarized the current research advances of immunotherapeutic biomarkers in pancreatic cancer, hoping to help clinicians understand relevant biomarkers systematically and guide the precise treatment of pancreatic cancer.

Tumor immunotherapeutics include immune checkpoint inhibitors, adoptive cellular therapy, tumor vaccines, immunomodulators, which regulate or induce anti-tumor activity by blocking immunosuppressive signals, infusing in vitro-induced anti-tumor effector cells, and enhancing the immunogenicity of tumor cells in the fight against cancer. The effect mechanisms of tumor immunotherapy is different from that of other tumor therapeutic approaches, such as surgery and chemotherapy. Therefore, in the evaluation of anti-tumor efficacy, the use of conventional imaging methods to detect the volume change of tumor lesions shows special response patterns such as “false progression” and “superprogression”, which cannot timely and accurately evaluate the objective efficacy of tumor immunotherapy. This review is an attempt to focus on those challenges in evaluating immunotherapy efficacy and the latest developments of relevant evaluation criteria, and is aimed at providing reference for the scientific evaluation of tumor immunotherapy efficacy and the selection of appropriate immunotherapy strategies for tumor patients.

Objective: To investigate the expression pattern, clinical significance, and the regulatory role of 2', 5'-oligoadenylate synthetase 1 (OAS1) in the proliferation of pancreatic ductal adenocarcinoma (PDAC) cells.

Methods: Public databases such as Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) were used to analyze the expression of OAS1 in pancreatic cancer tissues. Immunohistochemical staining was applied to validate the expression level of OAS1 in PDAC tissue microarrays, and the association between OAS1 expression level and the prognosis of patients was analyzed. Real-time fluorescence quantitative PCR was performed to examine the expression level of OAS1 mRNA in different PDAC cell lines. CCK-8 assay and colony formation assay was used to assess the effect of OAS1 on the proliferation of PDAC cells after OAS1 silencing in Patu-8988 and PDC0034 cells by siRNA treatment. Further, Gene Set enrichment analysis (GSEA) was performed to screen for possible molecular mechanism of the regulatory role of OAS1 in PDAC. Cell viability and cholesterol level was analyzed after treatment with mTOR signaling activator MHY1485 in OAS1-silenced Patu-8988 and PDC0034 cells in order to verify the underlying mechanism of the regulatory role of OAS1 in PDAC cell proliferation.

Results: Database analysis showed significant upregulation of OAS1 expression in pancreatic cancer tissues (P < 0.05). Immunohistochemical staining results from PDAC tissues microarray showed that OAS1 expression was significantly upregulated in PDAC tissues compared with the paired paracancerous tissues, and high OAS1 expression was associated with poor prognosis (P < 0.05). Real-time fluorescence quantitative PCR and Western blotting analysis show that OAS1 expression was higher in PDAC cells lines compared with normal ductal cells of the pancreas. The proliferative activity of PDAC cells decreased significantly after OAS1 silencing in Patu-8988 and PDC0034 cells (P < 0.001). GSEA results indicated that OAS1 may affect PDAC cell proliferation through mTOR signaling pathway and cholesterol metabolism associated pathway. The mTOR signaling pathway may be inhibited and the total cellular cholesterol decreased after OAS1 silencing. Treatment with mammalian target of rapamycin (mTOR) activator MHY1485 partially reversed the inhibitory effect of OAS1 silencing on the proliferation and cholesterol metabolism of PDAC cells.

Conclusion: OAS1 expression is upregulated in PDAC tumor tissues and cells and is associated with poor prognosis. OAS1 may promote the proliferation of pancreatic cancer cells by enhancing cholesterol metabolism through activation of the mTOR signaling pathway.

Lung cancer is one of the most prevalent and the highest mortality rate malignancies, and its treatment landscape has undergone a disruptive transformation with the discovery and clinical application of immune checkpoint inhibitors. However, there still exists a number of patients who acquire resistance or fail to respond to these treatments, posing new challenges for lung cancer therapy. In light of this, there is an urgent need to actively explore and develop novel targets and innovative therapeutic strategies. This article aims to review the cutting-edge advancements in the novel immune checkpoint inhibitors, agonists, bispecific antibodies, adoptive cellular immunotherapy, and combination therapies involving immune checkpoint inhibitors, as well as to revisit existing related clinical trials along with their limitations, with the goal of advancing lung cancer immunotherapy towards a more personalized and precise approach.

The rapid development of the comprehensive intersection of oncology disciplines makes oncology teaching complex and challenging. In recent years, the deep integration of artificial intelligence (AI) and medical education has brought new opportunities for oncology teaching. Therefore, this paper proposes to construct a new teaching model of AI-enabled problem-based learning (PBL) fused with case-based learning (CBL), which fully combines PBL, CBL, virtual simulation technology, intelligent robots, AI models and other teaching methods, and integrates these innovative elements into all aspects of oncology teaching, including theoretical courses, laboratory operations and clinical practice, in order to provide a comprehensive and interactive oncology teaching system. This new teaching mode brings a new perspective and approach to theoretical, experimental, and clinical teaching in oncology, which not only helps to deepen students’ understanding of the basics of oncology, but also significantly improves their clinical thinking and problem-solving abilities. In addition, this new attempt at an integrated teaching method will provide a new teaching strategy for the development of medical oncology education.

The incidence and mortality of colorectal cancer (CRC) have been increasing year by year, and liver metastasis is the main cause of death for CRC patients. Approximately 49% of CRC patients died of liver metastasis, and about 25% of them developed liver metastasis after radical resection. The interaction between various cytokines (such as chemokines, exosomes) and immune cells in the tumor microenvironment (TME) is essential for tumor metastasis. So far, the mechanism of colorectal liver metastases (CRLM) has not been fully elucidated, but some studies have shown that CRLM does not only occur in the late stage of CRC, but also in the early stage of some patients. In this paper, we summarized the current understanding of CRLM pathogenesis from genomics, pathology, and TME perspectives. And we also reviewed the latest molecular regulatory mechanisms of CRLM, as well as the mechanisms of immune cells and cytokines related to TME. Finally, the latest research findings of CRLM immunotherapy are summarized, in order to provide new insights into the comprehensive treatment for CRLM patients.

Advanced gastric cancer (AGC) includes locally unresectable gastric cancer (GC), metastatic GC, and postoperative recurrent GC. Due to delayed diagnosis and lack of effective treatment for AGC, the median survival time of AGC patients is only 6-12 months. At present, the main treatment goal of AGC is to improve symptoms and prolong the survival time of patients receiving sequential chemotherapy. Although the therapeutic effect of systemic therapy on AGC is gradually becoming apparent, the patient's prognosis is far from expected. In addition, targeted therapy and novel immunotherapy have drawbacks such as high incidence of drug resistance, high toxic side effects, and heavy economic burden on patients. Therefore, finding new therapeutic targets and developing anti-tumor drugs is a key issue that urgently needs to be addressed. According to reports, abnormal activation of the hepatocyte growth factor (HGF)/ cellular-mesenchymal epithelial transition factor (c-MET) pathway plays a crucial role in the progression of GC and the occurrence of multi-line resistance and may be a potential therapeutic target for GC. In recent years, some HGF/c-MET-targeting small molecule tyrosine kinase inhibitors (TKIs) have been found to show good clinical effects in the treatment of GC. Meanwhile, new HGF/c-MET inhibitors (such as monoclonal antibodies, bispecific antibodies, antibody drug conjugates, etc.) have shown good anti-tumor activity in preclinical studies, but they are all at different stages of clinical research, and their efficacy and safety still need further confirmation. This review elaborates on the latest research progress of HGF/c-MET inhibitors in the treatment of AGC and discusses the main reasons and strategies for drug resistance, aiming to provide better guidance for the treatment of AGC and provide reference for future research.

Neurofibromatosis type 1 is a progressive autosomal dominant inherited disease caused by a mutation in neurofibromin 1 (NF1) gene located on chromosome 17q11.2. NF1 can cause systemic peripheral neuropathy, but the clinical manifestations are varied due to the different onset times and lesion sites in different patients. The treatment of NF1 involves multiple disciplines due to different lesion sites. Clinical monitoring and symptomatic treatment are the main methods for NF1 management, while radical treatment is difficult. New drugs targeted at the pathogenic gene-related signaling pathways are expected to improve the therapeutic effect for NF1. This review summarizes the progress in the basic research and clinical diagnosis and treatment of NF1.

Colon cancer is a common malignant tumor in the gastrointestinal tract, with morbidity and mortality rates increasing every year. Currently, the etiology of colon cancer has not been fully elucidated. With the deepening of colon cancer research and treatment, it is especially important to establish corresponding preclinical in vivo models. In the treatment of colon cancer, Chinese medicine follows the principle of diagnosis and treatment, adopts the method of supporting the positive and dispelling the evil, adjusts the body's qi and blood, and the deficiency of internal organs to maintain the balance of the body's yin and yang, so as to achieve the purpose of anti-tumor. Chinese medicine animal models of colon cancer can be broadly divided into five categories: damp-heat accumulation, qi stagnation and blood stasis, qi and blood deficiency, spleen and kidney yang deficiency and liver and kidney yin deficiency. Western animal models of colon cancer are commonly divided into 4 categories: spontaneous, induced, transplanted and genetically engineered. The paper summarizes the construction methods and characteristics of colon cancer animal models currently commonly used in Chinese and western medicine, and summarizes, analyzes and concludes the colon cancer animal models based on three aspects: how to select animal models, comparison of Chinese and western medicine modeling methods and evaluation of modeling success, with a view to finding suitable modeling methods for preclinical experiments, so as to provide guidance for the selection of animal models of colon cancer.