The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway is a prominent target in cancer immunotherapy. The highly heterogeneous and dynamically plastic nature of the tumor immune microenvironment (TIME) dictates the outcomes of immunotherapeutic interventions. Although the cGAS-STING pathway has been extensively studied in tumor immunity, current reviews predominantly focus on canonical linear signaling or cell-autonomous functions within isolated immune or tumor cell types, thereby failing to establish an integrated mechanistic framework that accounts for coordinated crosstalk among malignant, immune, and stromal compartments. Here, we move beyond the conventional paradigm of ligand-dependent, cell-intrinsic STING activation and instead adopt a systems-level perspective grounded in spatiotemporal context and dynamic regulation. We systematically delineate how cGAS-STING activity exerts context-dependent, non-cell-autonomous effects across the multicellular TIME network-functioning not as a generic immune amplifier, but as a regulatory axis that orchestrates immune-ecological reconfiguration of the microenvironment. Accordingly, we argue that next-generation therapeutic strategies should transition from indiscriminate pathway activation toward precision-targeted intervention and microenvironmental reprogramming-thereby enabling rational design of more effective and durable cancer immunotherapies.

The crosstalk among pyroptosis, apoptosis, and necroptosis has facilitated the emergence of the innovative concept of PANoptosis. As a form of immunogenic cell death, PANoptosis is closely associated with various tumors through its unique regulatory mechanisms, thereby offering novel directions and insights for tumor immunotherapy. This review summarizes the mechanistic underpinnings of PANoptosis and the current evidence regarding its role in tumor progression. Furthermore, we discuss immunotherapeutic strategies targeting PANoptosis, with the aim of transitioning the research paradigm of tumor cell death from a unimodal to a multidimensional regulatory framework, and providing new perspectives for the clinical management of malignancies.

Colorectal cancer (CRC) poses a significant challenge to public health worldwide. Mounting evidence implicates fatty liver disease as an accelerator of CRC. This study investigated the association between the Framingham Steatosis Index (FSI), also known as the Fatty Liver Substitution Index, and CRC susceptibility. This study aims to provide a theoretical foundation for developing preventive strategies and therapeutic interventions for individuals at high risk of CRC, thereby ultimately improving treatment outcomes. This study employed 1,01,316 baseline records from the NHANES database (1999-2018). The application of stringent eligibility criteria yielded 42,732 qualified subjects: 274 individuals with CRC and 42,458 control individuals. FSI quantification was performed using standardized procedures. Following covariate adjustment, analyses were performed using multivariate logistic regression, restricted cubic spline models, and stratification approaches to ascertain the relationship between FSI scores and CRC susceptibility. Within crude models, increased FSI levels were positively associated with CRC susceptibility, maintaining this direct association after covariate adjustment. Subgroup evaluations generated uniformly consistent findings across population categories, confirming the robustness of the findings. Dose-response analyses revealed a significant linear correlation, in which an increase in FSI magnitude corresponded to a heightened CRC probability. Increasing FSI levels increase the risk of developing CRC, providing new theoretical support for the diagnosis and treatment of CRC. However, cross-sectional studies aim to establish associations, and the causal relationship between the 2 requires further research to validate and assess the feasibility of applying these findings in clinical practice.

Benzo(a)pyrene (BaP), an environmental carcinogen, contributes to colon cancer pathogenesis through incompletely elucidated mechanisms. This study integrated network toxicology and multi-omics analyses to decipher BaP-associated molecular signatures and clinical relevance in colon cancer. Using TCGA-COAD data, 113 differentially expressed BaP-related targets were identified via CTD and Super-PRED databases. PPI networks, functional enrichment, and Cox/Lasso regression revealed key pathways (xenobiotic metabolism, p53 signaling, cell cycle) and six prognostic genes (CLK2, CRYAB, RPS6KA1, DPP7, CDC25C, GAST). A BaP-related risk model stratified patients into distinct survival groups. A nomogram accurately predicted 1-, 3-, and 5-year overall survival. High-risk scores correlated with advanced tumor stage, metastasis, and immunosuppressive microenvironments. Molecular docking demonstrated strong BaP binding to CLK2 and CRYAB. External validation (GSE39582, TNMplot) confirmed tumor-specific gene expression patterns. These findings delineate BaP-driven networks connecting xenobiotic stress, immune dysregulation, and tumor progression. The risk model provides a prognostic biomarker for personalized management and therapeutic targeting in colon cancer.

The convergence and interplay of pyroptosis, apoptosis, and necroptosis have led to the conceptualization of PANoptosis, an innovative paradigm of inflammatory programmed cell death. Characterized by the hierarchical assembly and activation of the PANoptosome, PANoptosis operates through tightly orchestrated signaling hubs and is intricately linked to organelle functionality. Accumulating evidence underscores its pivotal role in diverse oncogenic processes, positioning PANoptosis as a compelling frontier for antitumor therapeutic exploration. This review delineates the mechanistic underpinnings of PANoptosis, synthesizes its established contributions to tumor progression, and examines its dynamic crosstalk with the tumor immune microenvironment (TIME). Notably, we highlight recent breakthroughs in PANoptosis-driven immunotherapeutic strategies. We further propose that targeting PANoptosis to reprogram TIME represents a transformative approach in oncology, shifting the research paradigm from unimodal cell death regulation to multidimensional intervention. This perspective not only advances fundamental understanding but also holds significant promise for clinical translation, heralding a new era in cancer therapeutics.

Lung cancer is one of the leading causes of cancer-related deaths worldwide, with non-small cell lung cancer (NSCLC) accounting for 84% of cases. Traditional treatments like surgery and chemotherapy have limited effectiveness and significant side effects. Despite combination chemotherapy being the preferred first-line therapy, the prognosis for advanced NSCLC remains poor, with a median survival of 8-11 months and a 1-year survival rate of 30%. There is a critical need for new treatments targeting the molecular mechanisms of NSCLC. Precision medicine, or targeted therapy, has emerged as a promising approach, focusing on genetic and epigenetic alterations. This method is more effective for advanced NSCLC. It involves drugs targeting specific genetic abnormalities such as ROS proto-oncogene 1 (ROS1), EGFR (Epidermal growth factor receptor), ALK (Anaplastic lymphoma kinase), BRAF (v-Raf murine sarcoma viral oncogene homolog B1, MET (Mesenchymal epithelial transcription factor), and RET (Rearranged during transfection) mutations, which are vital driver genes for lung cancer development and progression. With up to twenty treatments approved by the FDA, targeted medicines are still being developed, and targeted therapy and chemotherapy have dramatically improved patient outcomes. Despite progress, treating metastatic NSCLC remains challenging due to resistance to genetic changes. This narrative review provides a detailed description of the various classifications of molecular targeted therapeutic approaches employed in lung cancer management and its mechanisms of action in cancer prevention and its advantages and disadvantages.

Colorectal cancer (CRC) is a diverse disease entity and a leading cause of cancer-related mortality worldwide. CRC results from the accumulation of multiple genetic and epigenetic alterations. This heterogeneity of CRC underscores the significance of understanding its molecular landscape, as variations in tumor genetics can greatly influence both patient prognosis and therapeutic response. The molecular complexity of CRC is defined by three major carcinogenesis pathways: chromosomal instability (CIN), microsatellite instability (MSI), and the CpG island methylator phenotype (CIMP). These pathways contribute to the onset and progression of CRC through mutations, epigenetic modifications, and dysregulated cellular signalling networks. The heterogeneous nature of CRC continues to pose challenges in identifying universally effective treatments, highlighting the need for personalized approaches. Hence, the present review aims at unravelling the molecular complexity of CRC that is essential for improving diagnosis, prognostication, and treatment. We detail on the current understanding of the molecular framework of CRC, central signalling pathways of CRC associated with its initiation to a malignant phenotype, further invasion, progression, metastases, and response to therapy. Continued research into CRC's pathways and biomarkers will pave the way for the development of more precise and effective therapeutic strategies, ultimately improving patient outcomes.

The immune system has a substantial impact on the growth and expansion of lung malignancies. Immune cells are encompassed by a stroma comprising an extracellular matrix (ECM) and different cells like stromal cells, which are known as the tumor immune microenvironment (TIME). TME is marked by the presence of immunosuppressive factors, which inhibit the function of immune cells and expand tumor growth. In recent years, numerous strategies and adjuvants have been developed to extend immune responses in the TIME, to improve the efficacy of immunotherapy. In this comprehensive review, we outline the present knowledge of immune evasion mechanisms in lung TIME, explain the biology of immune cells and diverse effectors on these components, and discuss various approaches for overcoming suppressive barriers. We highlight the potential of novel adjuvants, including toll-like receptor (TLR) agonists, cytokines, phytochemicals, nanocarriers, and oncolytic viruses, for enhancing immune responses in the TME. Ultimately, we provide a summary of ongoing clinical trials investigating these strategies and adjuvants in lung cancer patients. This review also provides a broad overview of the current state-of-the-art in boosting immune responses in the TIME and highlights the potential of these approaches for improving outcomes in lung cancer patients.

Specific protein 1 (Sp1) is central to regulating transcription factor activity and cell signaling pathways. Sp1 is highly associated with the poor prognosis of various cancers; it is considered a non-oncogene addiction gene. The function of Sp1 is complex and contributes to regulating extensive transcriptional activity, apart from maintaining basal transcription. Sp1 activity and stability are affected by post-translational modifications (PTMs), including phosphorylation, ubiquitination, acetylation, glycosylation, and SUMOylation. These modifications help to determine genetic programs that alter the Sp1 structure in different cells and increase or decrease its transcriptional activity and DNA binding stability in response to pathophysiological stimuli. Investigating the PTMs of Sp1 will contribute to a deeper understanding of the mechanism underlying the cell signaling pathway regulating Sp1 stability and the regulatory mechanism by which Sp1 affects cancer progression. Furthermore, it will facilitate the development of new drug targets and biomarkers, thereby elucidating considerable implications in the prevention and treatment of cancer.

目的 探讨智能超声引导两步法建立标准通道经皮肾镜碎石术治疗上尿路结石的临床效果.方法 选择吉林医药学院附属医院泌尿外科2021年1月-12月收治42例上尿路结石患者为研究对象,应用智能超声引导两步法建立标准通道经皮肾镜取石术治疗,回顾临床病例资料.结果 本组42例次一期成功建立通道完成手术.一期手术碎石率100％.单发结石清石率100％,多发结石与铸型结石清石率为73.2％,残留结石直径介于0.5～1.5 cm术后采用体外冲击波碎石或软镜治疗,均能达到临床治愈.术中和术后的并发症:接受输血治疗的患者2例,气胸1例,腹膜后尿或灌注液的外渗有2例,发热5例,经抗炎治疗后治愈,未出现感染性休克的病例.结论 采用智能超声引导两步法建立标准通道经皮肾镜碎石术治疗上尿路结石,手术操作时间短,手术创伤小,结石碎石率、清石率高,严重手术并发症发生率低,值得临床推广应用.

Objective:To analyze and explore the possible mechanism of anti-tumor metastasis of Notoginseng Radix et Rhizoma using Internet pharmacology. Methods:The active components and targets of Notoginseng Radix et Rhizoma were screened by retrieving Chinese Medicine System Pharmacology Database and Analysis Platform (TCMSP). GeneCards database was used to screen the anti-tumor metastasis-related targets, and compounds and disease targets were under mapping analysis. Key targets of Notoginseng Radix et Rhizoma for anti-tumor metastasis were screened through Venn map. With the help of Cytoscape 3.7.2 software, a compound-disease network diagram was constructed. String platform was used to build a PPI network. Bioconductor was used to enrich the target genes for KEGG signaling pathway and GO biological process analysis. Results:Totally 119 active components were selected from Notoginseng Radix et Rhizoma. There were 8 eligible active components, corresponding to 162 related targets, 121 targets related to anti-tumor metastasis, and 30 key targets screened by PPI network, including AKT1, MAPK1, JUN, RELA, IL6, etc. GO enrichment analysis mainly involved biological processes such as cytokine receptor binding, heme binding, RNA polymerase Ⅱ transcription factor binding, ubiquitin protein ligase binding, and steroid hormone receptor activity. 149 signal pathways related to Notoginseng Radix et Rhizoma anti-tumor metastasis were obtained by KEGG enrichment analysis, mainly involving multiple signal pathways, such as AGE-RAGE and PI3K-Akt, and hepatitis B, Kaposi's sarcoma-associated herpes virus infection, human cytomegalovirus infection and other viral infections and various tumors. Conclusion:Notoginseng Radix et Rhizoma can pass multiple active components, such as ginsenoside f2, ginsenoside rh2 β-, sitosterol, stigmasterol and quercetin, and multiple targets, such as AKT1, MAPK1, JUN, RELA and IL6, acting on multiple pathways such as PI3K-Akt, thereby playing the role of anti-tumor metastasis.

嗜铬细胞瘤是来源于肾上腺或神经节嗜铬组织的一种功能性肿瘤,其中90％发生于肾上腺. 由于嗜铬组织可以自主分泌大量的儿茶酚胺,引起持续性或阵发性高血压、高代谢及高血糖等临床症状,最终导致多器官功能和代谢紊乱[1] ,大约 40％左右的病人平时血压正常,发作时血压突然升高,50％以上的病人在高血压基础上发作时血压极度升高,发作时收缩压甚至可以达到 200 ～300 mmHg (1 mmHg = 133 kPa),舒张压可以达到130 ～180 mmHg,多数病人还可表现为代谢紊乱,病人表现为血糖升高、脂代谢紊乱、低钾血症等.

目的 探讨麻黄-细辛药对提取物对哮喘小鼠模型气道重塑的影响.方法 将30只Balb/c小鼠分为对照组、模型组、麻黄-细辛组,各10只.除对照组外,其他两组建立哮喘小鼠模型.建模后第18天起给予麻黄-细辛组麻黄-细辛药对提取物雾化吸入治疗,给予对照组和模型组小鼠等体积生理盐水雾化吸入.观察各组小鼠肺组织形态,检测各组小鼠增强呼气间歇值(Penh),肺支气管肺泡灌洗液(BALF)中各类白细胞比例,BALF和血清的白细胞介素(IL)-6和IL-17水平,以及肺组织的Yes相关蛋白(YAP)、YAP mRNA、转化生长因子 β1(TGF-β1)蛋白、α-平滑肌肌动蛋白(α-SMA)的表达水平.结果 各组小鼠吸入相应浓度乙酰甲胆碱后,模型组小鼠Penh均高于对照组,麻黄-细辛组小鼠Penh均低于模型组(均P<0.05).模型组小鼠的BALF中嗜酸性粒细胞、淋巴细胞、单核细胞及中性粒细胞比例,BALF和血清中IL-6及IL-17水平,以及肺组织中TGF-β1蛋白和α-SMA表达水平,YAP及其mRNA表达水平均高于对照组(均P<0.05);与模型组比较,麻黄-细辛组上述指标水平均降低(均P<0.05).结论 麻黄-细辛药对提取物能够减轻哮喘模型小鼠的气道反应性和炎症反应,并可能通过下调IL-17、IL-6、TGF-β1、α-SMA、YAP等因子的表达而抑制哮喘模型小鼠的气道重塑.

目的 探讨输尿管上段结石致重度肾积水患者行一期肾造瘘二期造瘘管(由肾脏远端至近端)冲水输尿管镜碎石术治疗的临床效果.方法 选择2021 年2 月至12 月由于输尿管上段结石嵌顿过久所致的重度肾脏积水患者30 例,根据患者住院诊治期间采用的不同手术治疗方式分为对照组和观察组,每组各15 人.对照组采用传统输尿管镜碎石术治疗,观察组采用一期肾造瘘二期造瘘管(由肾脏远端至近端)逆行冲水输尿管镜碎石术治疗.比较两组治疗效果及愈后情况.结果 结石清除率观察组患者为 93.33%,对照组患者为73.33%;术后发热或炎性反应发生率观察组患者为 6.66%,对照组患者为26.66%.两组差异具有统计学意义(P＜0.05).结论 采用一期肾造瘘二期造瘘管(由肾脏远端至近端)冲水进行输尿管镜碎石术治疗输尿管上段结石嵌顿过久所导致的重度肾脏积水,结石清除率明显上升,能够有效避免术后发热或炎性反应的发生.

目的 探讨潞党参口服液防治气血两虚型肺癌患者化学药物治疗(简称化疗)所致骨髓抑制的临床疗效.方法 选取医院2019年1月至2020年12月收治的气血两虚型肺癌患者62例,按随机数字表法分为观察组和对照组,各31例.两组患者按肺癌病理类型不同给予对应化疗并口服鲨肝醇、护肝片等行常规治疗,视病情给予重组人粒细胞刺激因子(rhG-CSF)注射液皮下注射,观察组患者加服潞党参口服液.两组均以21 d为1个治疗周期,共治疗4个周期.结果 两组患者化疗4周期后的白细胞计数(WBC)均显著降低(P<0.01),观察组化疗2及4周期后均显著高于对照组(P<0.05,P<0.01);观察组患者rhG-CSF使用率及用量均显著低于对照组(P<0.01);观察组患者治疗后的中医证候积分显著降低(P<0.01),卡氏评分显著升高(P<0.05);两组患者骨髓抑制分级分布情况无显著差异,但观察组中重度(Ⅱ级及以上)骨髓抑制发生率显著低于对照组(41.94％比67.74％,P<0.05).结论 潞党参口服液能减轻气血两虚型肺癌患者化疗所致骨髓抑制的程度,维持白细胞计数,增强机体免疫功能,改善患者的中医证候,提高其生活质量.

导师隋博文主任在诊治特发性肺纤维化的过程中擅于运用"气血相生"理论进行辨证论治,认为"气虚血瘀、肺损络伤"为本病的基本病机.依据"气血相生"理论,"养血活血,以复肺气"为基本治疗原则,加以止咳化痰、宣肺平喘等治法来改善临床症状,同时注重后天脾胃的调养.治疗上运用桃红四物汤进行加减变化,收效良好.笔者通过探讨气血的来源以及肺脏功能结构与气血之间的关系,对导师治疗特发性肺纤维化这一临床经验进行分析、总结,以期为今后治疗特发性肺纤维化提供一定的思路.

目的 应用数据挖掘和聚类分析总结刘松江治疗乳腺癌学术思想和辨证思路.方法 将患者基本信息、四诊、诊断及治疗等病历信息录入中国中医科学院提供的中医传承辅助平台(V3.0),建立刘松江治疗乳腺癌的医案数据库.并以此数据库为基础,运用关联规则分析、改进的互信息法、复杂系统熵聚类等方法进行数据统计和分析.结果 通过对98首处方,194味药物的功效统计,使用频次最多的为补虚药,通过关联规则分析常用药对及置信度得到核心处方,利用聚类分析得到4个类方.结论 总结刘松江治疗乳腺癌调理阴阳,以"和"为贵,重视整体兼顾局部的学术思想.

Objective:To perform gene set enrichment analysis (GSEA) and analysis of immune cell infiltration on non-small-cell lung cancer (NSCLC) expression profiling microarray data based on bioinformatics, construct TICS scoring model to distinguish prognosis time, screen key genes and cancer-related pathways for NSCLC treatment, explore differential genes in NSCLC patients, predict potential therapeutic targets for NSCLC, and provide new directions for the treatment of NSCLC. Methods:Transcriptome data of 81 NSCLC patients and the GEO database were used to download matching clinical data (access number: GSE120622). Form the expression of non-small cell lung cancer (NSCLC). TICS values were calculated and grouped according to TICS values, and we used mRNA expression profile data to perform GSEA in non-small-cell lung cancer patients. Biological process (GO) analysis and DAVID and KOBAS were used to undertake pathway enrichment (KEGG) analysis of differential genes. Use protein interaction (PPI) to analyze the database STRING, and construct a PPI network model of target interaction. Results:We obtained 6 significantly related immune cells including activated B cells through the above analysis (Figure 1(b), p < 0.001). Based on the TICS values of significantly correlated immune cells, 41 high-risk and 40 low-risk samples were obtained. TICS values and immune score values were subjected to Pearson correlation coefficient calculation, and TICS and IMS values were found to be significantly correlated (Cor = 0.7952). Based on non-small-cell lung cancer mRNA expression profile data, a substantial change in mRNA was found between both the high TICS group as well as the low TICS group (FDR 0.01, FC > 2). The researchers discovered 730 mRNAs that were considerably upregulated in the high TICS group and 121 mRNAs that were considerably downregulated in the low TICS group. High confidence edges (combined score >0.7) were selected using STRING data; then, 191 mRNAs were matched to the reciprocal edges; finally, an undirected network including 164 points and 777 edges was constructed. Important members of cellular chemokine-mediated signaling pathways, such as CCL19, affect patient survival time. Conclusion:(1) The longevity of patients with non-small-cell lung cancer was substantially connected with the presence of immature B cells, activated B cells, MDSC, effector memory CD4 T cells, eosinophils, and regulatory T cells. (2) Immune-related genes such as CX3CR1, CXCR4, CXCR5, and CCR7, which are associated with the survival of NSCLC, affect the prognosis of NSCLC patients by regulating the immune process.

Application of the anticancer drug doxorubicin (DOX) is restricted due to its adverse, cardiotoxic side effects, which ultimately result in heart failure. Moreover, there are a limited number of chemical agents for the clinical prevention of DOX-induced cardiotoxicity. Based on the theories of traditional Chinese medicine (TCM) on chronic heart failure (CHF), Shenlijia (SLJ), a new TCM compound, has been developed to fulfill multiple functions, including improving cardiac function and inhibiting cardiac fibrosis. In the present study, the protective effects and molecular mechanisms of SLJ on DOX-induced CHF rats were investigated. The CHF rat model was induced by intraperitoneal injection of DOX for six weeks with the cumulative dose of 15 mg/kg. All rats were then randomly divided into the control, CHF, CHF + SLJ (3.0 g/kg per day), and CHF + captopril (3.8 mg/kg per day) groups and treated for further four weeks. Echocardiography and the assessment of hemodynamic parameters were performed to evaluate heart function. A protein chip was applied to identify proteins with diagnostic values that were differentially expressed following SLJ treatment. The data from these investigations showed that SLJ treatment significantly improved cardiac function by increasing the left ventricular ejection fraction, improving the hemodynamic index, and inhibiting interstitial fibrosis. Protein chip analysis revealed that SLJ upregulated MCP-1, MDC, neuropilin-2, TGF-β3, thrombospondin, TIE-2, EG-VEGF/PK1, and TIMP-1/2/3 expressions and downregulated that of MMP-13. In addition, immunohistochemistry and western blot results further confirmed that SLJ promoted TIMP-1/2/3 and inhibited MMP-13 expression. The results of the present study suggest that SLJ was effective against DOX-induced CHF rats and is related to the improvement of heart function and ultrastructure and the inhibition of myocardial fibrosis.