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Depression is a prevalent and intricate mental disorder. The involvement of small RNA molecules, such as microRNAs in the pathogenesis and neuronal mechanisms underlying the depression have been documented. Previous studies have demonstrated the involvement of microRNA-143-3p (miR-143-3p) in the process of fear memory and pathogenesis of ischemia; however, the relationship between miR-143-3p and depression remains poorly understood. Here we utilized two kinds of mouse models to investigate the role of miR-143-3p in the pathogenesis of depression. Our findings reveal that the expression of miR-143-3p is upregulated in the ventral hippocampus (VH) of mice subjected to chronic restraint stress (CRS) or acute Lipopolysaccharide (LPS) treatment. Inhibiting the expression of miR-143-3p in the VH effectively alleviates depressive-like behaviors in CRS and LPS-treated mice. Furthermore, we identify Lasp1 as one of the downstream target genes regulated by miR-143-3p. The miR-143-3p/Lasp1 axis primarily affects the occurrence of depressive-like behaviors in mice by modulating synapse numbers in the VH. Finally, miR-143-3p/Lasp1-induced F-actin change is responsible for the synaptic number variations in the VH. In conclusion, this study enhances our understanding of microRNA-mediated depression pathogenesis and provides novel prospects for developing therapeutic approaches for this intractable mood disorder.
Subject(s)
Cytoskeletal Proteins , Depression , Hippocampus , MicroRNAs , Animals , MicroRNAs/genetics , MicroRNAs/metabolism , Hippocampus/metabolism , Mice , Depression/metabolism , Depression/genetics , Male , Cytoskeletal Proteins/genetics , Cytoskeletal Proteins/metabolism , Mice, Inbred C57BL , LIM Domain Proteins/genetics , LIM Domain Proteins/metabolism , Behavior, Animal , Disease Models, Animal , Stress, Psychological/metabolism , Gene Expression RegulationABSTRACT
Pancreatic cancer is an aggressive cancer with a poor prognosis. Metabolic abnormalities are one of the hallmarks of pancreatic cancer, and pancreatic cancer cells can adapt to biosynthesis, energy intake, and redox needs through metabolic reprogramming to tolerate nutrient deficiency and hypoxic microenvironments. Pancreatic cancer cells can use glucose, amino acids, and lipids as energy to maintain malignant growth. Moreover, they also metabolically interact with cells in the tumour microenvironment to change cell fate, promote tumour progression, and even affect immune responses. Importantly, metabolic changes at the body level deserve more attention. Basic research and clinical trials based on targeted metabolic therapy or in combination with other treatments are in full swing. A more comprehensive and in-depth understanding of the metabolic regulation of pancreatic cancer cells will not only enrich the understanding of the mechanisms of disease progression but also provide inspiration for new diagnostic and therapeutic approaches.
Subject(s)
Pancreatic Neoplasms , Tumor Microenvironment , Humans , Pancreatic Neoplasms/metabolism , Pancreatic Neoplasms/pathology , Pancreatic Neoplasms/genetics , Animals , Energy MetabolismABSTRACT
Robot-assisted laparoscopic radical prostatectomy (RALP) has emerged as an effective treatment for prostate cancer with obvious advantages. This study aims to identify risk factors related to hypoxemia during the emergence from anesthesia in patients undergoing RALP. A cohort of 316 patients undergoing RALP was divided into two groups: the hypoxemia group (N = 134) and the non-hypoxemia group (N = 182), based on their postoperative oxygen fraction. Comprehensive data were collected from the hospital information system, including preoperative baseline parameters, intraoperative data, and postoperative recovery profiles. Risk factors were examined using multiple logistic regression analysis. The study showed that 38.9% of patients had low preoperative partial pressure of oxygen (PaO2) levels. Several clinical parameters showed significant differences between the hypoxemia group and the non-hypoxemia group, including weight (P < 0.0001), BMI (P < 0.0001), diabetes mellitus (P = 0.044), history of emphysema and pulmonary alveoli (P < 0.0001), low preoperative PaO2 (P < 0.0001), preoperative white blood cell count (P = 0.012), preoperative albumin (P = 0.048), intraoperative bleeding (P = 0.043), intraoperative CO2 accumulation (P = 0.001), duration of surgery (P = 0.046), postoperative hemoglobin level (P = 0.002), postoperative hypoxemia (P = 0.002), and early postoperative fever (P = 0.006). Multiple logistic regression analysis revealed BMI (adjusted odds ratio = 0.696, 95% confidence interval 0.612-0.719), low preoperative PaO2 (adjusted odds ratio = 9.119, 95% confidence interval 4.834-17.203), and history of emphysema and pulmonary alveoli (adjusted odds ratio = 2.804, 95% confidence interval 1.432-5.491) as independent factors significantly associated with hypoxemia on emergence from anesthesia in patients undergoing RALP. Our results demonstrate that BMI, lower preoperative PaO2, and a history of emphysema and pulmonary alveolar disease are independent risk factors associated with hypoxemia on emergence from anesthesia in patients undergoing RALP. These findings provide a theoretical framework for surgeons and anesthesiologists to facilitate strategies to mitigate postoperative hypoxemia in this unique patient population.
Subject(s)
Hypoxia , Laparoscopy , Postoperative Complications , Prostatectomy , Prostatic Neoplasms , Robotic Surgical Procedures , Humans , Prostatectomy/methods , Prostatectomy/adverse effects , Robotic Surgical Procedures/methods , Robotic Surgical Procedures/adverse effects , Male , Hypoxia/etiology , Risk Factors , Laparoscopy/methods , Laparoscopy/adverse effects , Middle Aged , Aged , Prostatic Neoplasms/surgery , Postoperative Complications/etiology , Postoperative Complications/epidemiology , Postoperative Complications/prevention & control , Anesthesia Recovery Period , Anesthesia/methodsABSTRACT
Purpose: Transcutaneous electrical acupoint stimulation (TEAS) can be used in patients with infertility. This study explored the impact of TEAS on brain-derived neurotrophic factor (BDNF) levels and in-vitro fertilization (IVF) outcomes in patients with infertility. Patients and Methods: This quasi-experimental study included infertile women undergoing IVF and embryo transfer (IVF-ET) at one hospital between January 2018 and December 2021. The TEAS group received TEAS before IVF, while the placebo group received mock stimulation. The primary outcomes were serum and follicular fluid (FF) BDNF expression levels. Finally, 510 and 518 participants were included in TEAS and placebo groups. Results: The serum (P<0.001) and FF (P<0.001) BDNF expression levels were higher in the TEAS group than in the placebo group. The TEAS group had a lower total dose of gonadotropins (P=0.007), higher fertilization rates (P=0.006), higher high-quality embryo rates (P=0.013), and higher pregnancy rates per ET (P=0.031). The subgroup analysis showed that the Val/Val genotype was associated with the differences in serum and FF BDNF between the TEAS and placebo groups (all P<0.05). Conclusion: In conclusion, TEAS might increase serum and FF BDNF expression levels and improve IVF embryological and clinical outcomes. Patients with the Val/Val genotype might be more likely to benefit from TEAS.
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OBJECTIVES: The aim of the present study was to evaluate the results of isolated coronary artery bypass grafting (CABG) with or without revascularization of the occluded right coronary artery (RCA). METHODS: Patients undergoing isolated CABG were included in a prospective European multicenter registry. Outcomes were adjusted for imbalance in preoperative variables with propensity score matching analysis. Late outcomes were evaluated with Kaplan-Meier's method and competing risk analysis. RESULTS: Out of 2,948 included in this registry, 724 patients had a total occlusion of the RCA and were the subjects of this analysis. Occluded RCA was not revascularized in 251 (34.7%) patients with significant variability between centers. Among 245 propensity score-matched pairs, patients with and without revascularization of occluded RCA had similar early outcomes. The nonrevascularized RCA group had increased rates of 5-year all-cause mortality (17.7 vs. 11.7%, p = 0.039) compared with patients who had their RCA revascularized. The rates of myocardial infarction and repeat revascularization were only numerically increased but contributed to a significantly higher rate of MACCE (24.7 vs. 15.7%, p = 0.020) at 5 year among patients with nonrevascularized RCA. CONCLUSION: In this multicenter study, one-third of totally occluded RCAs was not revascularized during isolated CABG for multivessel coronary artery disease. Failure to revascularize an occluded RCA in these patients increased the risk of all-cause mortality and MACCEs at 5 years.
Subject(s)
Coronary Artery Disease , Percutaneous Coronary Intervention , Humans , Prospective Studies , Treatment Outcome , Coronary Artery Bypass , Coronary Artery Disease/surgeryABSTRACT
BACKGROUND: Intratumoral microbial communities have been recently discovered to exist in a variety of cancers and have been found to be intricately involved in tumour progression. Therefore, investigating the profiles and functions of intratumoral microbial distribution in hepatocellular carcinoma (HCC) is imperative. METHODS: To verify the presence of microorganisms in HCC, we performed fluorescence in situ hybridization (FISH) using HCC tissues and conducted MiSeq using 99 HCC and paracancerous tissues to identify the key microorganisms and changes in metabolic pathways affecting HCC progression through a variety of bioinformatics methods. RESULTS: Microbial diversity was significantly higher in HCC tissues than in adjacent tissues. The abundances of microorganisms such as Enterobacteriaceae, Fusobacterium and Neisseria were significantly increased in HCC tissues, while the abundances of certain antitumour bacteria such as Pseudomonas were decreased. Processes such as fatty acid and lipid synthesis were significantly enhanced in the microbiota in HCC tissues, which may be a key factor through which intratumoral microbes influence tumour progression. There were considerable differences in the microbes and their functions within tumour tissue collected from patients with different clinical features. CONCLUSION: We comprehensively evaluated the intratumoral microbial atlas of HCC tissue and preliminarily explored the mechanism of the effects of the microbial community involving changes in lipid metabolism and effects on HCC progression, which lays the foundation for further research in this field.
Subject(s)
Carcinoma, Hepatocellular , Liver Neoplasms , Humans , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/pathology , Liver Neoplasms/genetics , Liver Neoplasms/pathology , In Situ Hybridization, Fluorescence , Computational BiologyABSTRACT
Electric agglomeration technology is effective in removing particulate matter from the environment and has been widely used in the field of dust removal. For the first time, this technology is applied to the field of fire smoke removal at lab scale. By varying applied electric potential and initial concentration of smoke, the removal characteristics and mechanisms during the electric agglomeration process are systematically studied. The results show that when the applied electric potential is higher than 4 kV, the smoke transmittance increases from 4% to 90% in just 10 s, and the threshold for people safe escape can be reached in only 5 s. Three main mechanisms involved in the process of smoke removal using electric agglomeration are proposed. In addition to the conventional Coulomb agglomeration of charged particles, the turbulence-enhanced agglomeration induced by ionic wind and dipole chainization at the grounded plate are also observed. This study demonstrates the feasibility and potential of electric agglomeration technology to remove fire smoke.
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Aberrant long noncoding RNA (lncRNA) expression and fatty acid signaling dysfunction both contribute to hepatocellular carcinoma (HCC) occurrence and development. However, the relationship and interaction mechanism between lncRNAs and fatty acid signaling in HCC remain unclear. Data regarding RNA expression and clinical outcomes for patients with HCC were obtained from The Cancer Genome Atlas (TCGA), HCCDB, and the Gene Expression Omnibus (GEO) databases. Hallmark pathways were identified using the single-sample gene set enrichment analysis (ssGSEA) method. ConsensusClusterPlus was used to establish a consistency matrix for classifying samples into three subtypes. A risk signature was established, and predictive values for key lncRNAs related to prognosis were evaluated using Kaplan-Meier analysis and receiver operating characteristic curves. The ESTIMATE algorithm, MCP-Counter, and ssGSEA were used to evaluate the characteristics of the tumor immune microenvironment. The CTRP2.0 and PRISM were used to analyze drug sensitivity in HCC subtypes. We discovered seven fatty-acid-associated lncRNAs with predictive prognostic capabilities, including TRAF3IP2-AS1, SNHG10, AL157392.2, LINC02641, AL357079.1, AC046134.2, and A1BG-AS. Three subtypes were obtained, which presented with differences in prognosis, clinical information, mutation features, pathway traits, immune characteristics, and drug sensitivity. The seven key lncRNAs identified in this study might serve as promising biomarkers for predicting prognosis in patients with HCC, and the three HCC subtypes classified according to lncRNA expression profiles could improve HCC classification.
Subject(s)
Carcinoma, Hepatocellular , Liver Neoplasms , RNA, Long Noncoding , Humans , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/pathology , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , Liver Neoplasms/genetics , Liver Neoplasms/pathology , Fatty Acids , Gene Expression Regulation, Neoplastic , Biomarkers, Tumor/genetics , Biomarkers, Tumor/metabolism , Prognosis , Tumor MicroenvironmentABSTRACT
Background: Single-cell sequencing (SCS) technologies enable analysis of gene structure and expression data at single-cell resolution. However, SCS analysis in pancreatic cancer remains largely unexplored. Methods: We downloaded pancreatic cancer SCS data from different databases and applied appropriate dimensionality reduction algorithms. We identified 10 cell types and subsequently screened differentially expressed marker genes of these 10 cell types using FindAllMarkers analysis. Also, we evaluated the tumor immune microenvironment based on ESTIMATE and MCP-counter. Statistical enrichment was evaluated using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis. We used all candidate gene sets in KEGG database to perform gene set enrichment analysis. We used LASSO regression to reduce the number of genes in the pancreatic risk model by R package glmnet, followed by rtPCR to validate the expression of the signature genes in different pancreatic cancer cell lines. Results: We identified 15 cell subpopulations by dimension reduction and data clustering. We divided the 15 subpopulations into 10 distinct cell types based on marker gene expression. Then, we performed functional enrichment analysis for the 352 marker genes in pancreatic cancer cells. Based on RNA expression data and prognostic information from TCGA and GEO datasets, we identified 42 prognosis-related genes, including 5 protective genes and 37 high-risk genes, which we used to identified two molecular subtypes. C1 subtype was associated with a better prognosis, whereas C2 subtype was associated with a worse prognosis. Moreover, chemokine and chemokine receptor genes were differentially expressed between C1 and C2 subtypes. Functional and pathway enrichment uncovered functional differences between C1 and C2 subtype. We identified eight genes that could serve as potential biomarkers for prognosis prediction in pancreatic cancer patients. These genes were used to establish an 8-gene pancreatic cancer prognostic model. Conclusions: We established an 8-gene pancreatic cancer prognostic model. This model can meaningfully predict prognosis and treatment response in pancreatic cancer patients.
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OBJECTIVES: The aim of the present study was to evaluate the risk of late mortality and major adverse cardiovascular and cerebral events after coronary artery bypass grafting (CABG) in patients with prior percutaneous coronary intervention (PCI). METHODS: A total of 2948 patients undergoing isolated CABGs were included in a prospective multicenter registry. Outcomes were adjusted for multiple covariates in logistic regression, Cox proportional hazards analysis and competing risk analysis. RESULTS: In all, 2619 patients fulfilled the inclusion criteria of this analysis. Of them, 2199 (79.1%) had no history of PCI and 420 (20.9%) had a prior PCI. An adjusted analysis showed that a single prior PCI and multiple prior PCIs did not increase the risk of 30-day and 5-year mortality. Patients with multiple prior PCIs had a significantly higher risk of 5-year myocardial infarction (SHR 2.566, 95%CI 1.379-4.312) and repeat revascularization (SHR 1.774, 95%CI 1.140-2.763). Similarly, 30-day and 5-year mortality were not significantly increased in patients with prior PCI treatment of single or multiple vessels. Patients with multiple vessels treated with PCI had a significantly higher risk of 5-year myocardial infarction (SHR 2.640, 95%CI 1.497-4.658), repeat revascularization (SHR 1.648, 95%CI 1.029-2.638) and stroke (SHR 2.215, 95%CI 1.056-4.646) at 5-year. The risk for repeat revascularization was also increased with a prior single vessel PCI, but not for other outcomes. CONCLUSIONS: Among patients undergoing CABGs, multiple prior PCIs seem to increase the risk of late myocardial infarction and the need for repeat revascularization, but not the risk of mortality.
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Single-photon emitters (SPEs) play an important role in many optical quantum technologies. However, an efficient large-scale approach to the generation of high-quality SPE arrays remains an elusive goal at room temperature. Here, we demonstrate a scalable method of generating SPE arrays in hexagonal boron nitride (hBN) with high yield, brightness, and purity using single-pulse irradiation by a femtosecond laser. Our use of a single pulse per defect pattern minimized heat-related damages and improved the purity of SPEs compared with the previous laser-based approaches. Under the optimized fabrication and post-treatment conditions, SPE arrays were successfully generated from the 3.0 µm defect patterns with 43% yield, the highest among the 2D-based top-down approaches. Importantly, we found that 100% of the bright defect patterns are SPEs with g2(0) < 0.5 under such conditions, with the lowest g2(0) = 0.06 ± 0.03. Our SPEs also exhibit the highest brightness with the saturation SPE rate at 7.15 million counts per second. We believe that our overall high-quality and large-scale approach will help a wide range of applications of SPEs in on-chip quantum technologies.
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Monolayer 2D semiconductors provide an attractive option for valleytronics due to valley-addressability. But the short valley-polarization lifetimes for excitons have hindered potential valleytronic applications. In this paper, we demonstrate a strategy for prolonging the valley-polarization lifetime by converting excitons to trions through efficient gate control and exploiting the much longer valley-polarization lifetimes for trions than for excitons. At charge neutrality, the valley lifetime of monolayer MoTe2 increases by a factor of 1000 to the order of nanoseconds from excitons to trions. The exciton-to-trion conversion changes the dominant depolarization mechanism from the fast electron-hole exchange for excitons to the slow spin-flip process for trions. Moreover, the degree of valley polarization increases to 38% for excitons and 33% for trions through electrical manipulation. Our results reveal the depolarization dynamics and the interplay of various depolarization channels for excitons and trions, providing an effective strategy for prolonging the valley polarization.
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As one of the most malignant cancers and despite various treatment breakthroughs, the prognosis of hepatocellular carcinoma (HCC) remains unsatisfactory. The immune status of the tumor microenvironment (TME) relates closely to HCC progression; however, the mechanism of immune cell infiltration in the TME remains unclear. In this study, we performed a new combination algorithm on lncRNA expression profile data from the TCGA-LIHC cohort to identify lncRNAs related to immune disorders. We identified 20 immune disorder-related lncRNAs and clustered HCC samples based on these lncRNAs. We identified four clusters with differences in immune cell infiltration and immune checkpoint gene expression. We further analyzed differences between groups 1 and 3 and found that the poor prognosis of group 3 may be due to specific and non-specific immunosuppression of the TME, upregulation of immune checkpoint pathways, and activation of tumor proliferation and migration pathways in group 3. We also developed a prognostic model and verified that it has good stability, effectiveness, and prognostic power. This study provides a basis for further exploration of the immune cell infiltration mechanism in HCC, differential HCC prognosis, and improvement of the efficacy of ICIs for the treatment of HCC.
Subject(s)
Carcinoma, Hepatocellular , Immune System Diseases , Liver Neoplasms , RNA, Long Noncoding , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/pathology , Gene Expression Regulation, Neoplastic , Humans , Immune System Diseases/genetics , Liver Neoplasms/genetics , Liver Neoplasms/pathology , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , Tumor Microenvironment/geneticsABSTRACT
Long non-coding RNAs (lncRNAs) play important roles in the occurrence and progression of tumors. Extensive research has contributed to the current understanding of the critical roles played by lncRNAs in various cancers. LncRNA MIR4435-2HG has been found to be crucial in many cancers, such as breast, cervical, colorectal, and gastric cancer. Expression of MIR4435-2HG is generally upregulated in cancers and MIR4435-2HG participates in many biological functions through molecular mechanism of competitive endogenous RNA networks. This review profiles recent research findings on the expression, functions, mechanism, and clinical value of MIR4435-2HG in cancer, and serves as a reference for further MIR4435-2HG-related research and clinical trials.
Subject(s)
MicroRNAs , RNA, Long Noncoding , Stomach Neoplasms , Gene Expression Regulation, Neoplastic , Humans , MicroRNAs/genetics , MicroRNAs/metabolism , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , Stomach Neoplasms/geneticsABSTRACT
BACKGROUND: Long non-coding RNAs regulate malignant behaviors of nasopharyngeal carcinoma (NPC). We aim to investigate the roles and mechanisms of long non-coding RNA maternally expressed gene 3 (lnc-MEG3) in NPC. METHODS: The expression levels of lnc-MEG3 and sequestosome 1 (SQSTM1) in NPC tissues and cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell invasion and migration abilities were evaluated using transwell and wound healing assays, respectively. RESULTS: Downregulated lnc-MEG3 expression and upregulated SQSTM1 expression were found in NPC tissues and cells. Overexpression of lnc-MEG3 inhibited invasion, migration, and epithelial-mesenchymal transition in NPC cells. Overexpression of lnc-MEG3 reduced the expression level of SQSTM1, and SQSTM1 expression was inversely correlated with lnc-MEG3 level in NPC tissues. Besides, overexpression of SQSTM1 reversed the effects of lnc-MEG3 overexpression. Moreover, knockdown of lnc-MEG3 enhanced NPC progression while its effects were eased by SQSTM1 silence. CONCLUSION: Lnc-MEG3 inhibits malignant behaviors by regulating SQSTM1 expression. It may serve as a therapeutic target to treat NPC.
Subject(s)
MicroRNAs , Nasopharyngeal Neoplasms , Cell Line, Tumor , Cell Movement , Cell Proliferation , Epithelial-Mesenchymal Transition , Gene Expression Regulation, Neoplastic , Humans , Nasopharyngeal Carcinoma/genetics , Nasopharyngeal Neoplasms/genetics , Neoplasm Invasiveness/genetics , Sequestosome-1 ProteinABSTRACT
A robust finite-time control (FTC) framework using continuous terminal sliding-mode control (SMC) and high-order sliding-mode observer (HOSMO) is discussed to realize the trajectory tracking of flexible-joint robots in this article. Control performances of the robots always suffer from unknown matched and mismatched time-varying disturbances. Traditional SMC exists with a chattering phenomenon and cannot cope with mismatched time-varying disturbances due to its inherent structure property. For this reason, two HOSMOs are devised to estimate the time-varying disturbances on the link and motor side, respectively. Then, by fusing the states and disturbance estimations into a novel terminal sliding-mode surface, a continuous robust FTC scheme is developed. The proposed control strategy can not only handle both matched and mismatched time-varying disturbances but also obtain a finite-time convergence performance. The rigorous finite-time stability analysis of the closed-loop system under the proposed control method is guaranteed. The results are illustrated to verify the effectiveness and robustness of the proposed design approach.
Subject(s)
Robotics , AlgorithmsABSTRACT
RNA methylation is considered a significant epigenetic modification, a process that does not alter gene sequence but may play a necessary role in multiple biological processes, such as gene expression, genome editing, and cellular differentiation. With advances in RNA detection, various forms of RNA methylation can be found, including N6-methyladenosine (m6A), N1-methyladenosine (m1A), and 5-methylcytosine (m5C). Emerging reports confirm that dysregulation of RNA methylation gives rise to a variety of human diseases, particularly hepatocellular carcinoma. We will summarize essential regulators of RNA methylation and biological functions of these modifications in coding and noncoding RNAs. In conclusion, we highlight complex molecular mechanisms of m6A, m5C, and m1A associated with hepatocellular carcinoma and hope this review might provide therapeutic potent of RNA methylation to clinical research.
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Pancreatic cancer is one of the malignant tumors with the worst prognosis in the world. As a new way of programmed cell death, ferroptosis has been proven to have potential in tumor therapy. In this study, we used the TCGA-PAAD cohort combined with the previously reported 60 ferroptosis-related genes to construct and validate the prognosis model and in-depth analysis of the differences in the function and immune characteristics of different RiskTypes. The results showed that the six-gene signature prognostic model that we constructed has good stability and effectiveness. Further analysis showed that the upregulated genes in the high-risk group were mainly enriched in extracellular matrix receptor-related pathways and other tumor-related pathways and the infiltration of immune cells, such as B, T, and NK cells, was suppressed. In short, our model shows good stability and effectiveness. Further studies have found that the prognostic differences between different RiskTypes may be due to the changes in the ECM-receptor pathway and activation of the immune system. Additionally, ICI drugs can treat pancreatic cancer in high-risk groups.