Breast cancer (BC) is a common malignancy with increasing annual incidence. Radiotherapy shows favorable clinical efficacy in BC management, but limited randomized controlled trial data is a major limitation. Therefore, further validation of the optimal radiotherapeutic strategy for early-stage BC is required. This network meta-analysis evaluated radiotherapy regimens’ effects on efficacy and cosmetic outcomes in early-stage BC, guiding clinical practice. A comprehensive literature search was conducted in PubMed, Cochrane Library, Embase, and Web of Science databases to identify randomized controlled trials and cohort studies investigating radiotherapy approaches for early-stage BC. Data screening and extraction were independently performed using a standardized protocol. Study quality was assessed using the Cochrane Risk of Bias tool and Newcastle–Ottawa Scale. The primary endpoint was ipsilateral breast recurrence (IBR), and secondary endpoints included locoregional recurrence, overall survival, disease-free survival, and cosmetic outcomes. Statistical analyses were performed using R 4.4.1 and STATA 18.0. A total of 36 studies involving 32,655 patients and 9 interventions were included. The lowest IBR rate was observed in patients treated with hypofractionated whole-breast irradiation (HF-WBI) (surface under the cumulative ranking curve [SUCRA], 10.54%), followed by conventional fractionated whole-breast irradiation (CF-WBI) (SUCRA, 35.70%). Compared with CF-WBI, intraoperative electron radiotherapy (IOeRT) (odds ratio [OR], 4.19; 95% credible interval [CrI], 1.83–10.26), intraoperative radiotherapy (IORT) (OR, 1.75; 95% CrI, 1.06–2.87), and HF-WBI (OR, 0.78; 95% CrI, 0.56–0.99) demonstrated statistically significant differences. The best cosmetic outcomes were achieved with three-dimensional conformal radiotherapy (3D-CRT) (SUCRA, 14.43%), followed by intensity-modulated radiotherapy (IMRT) (SUCRA, 16.04%). Compared with CF-WBI, 3D-CRT (OR, 0.11; 95% CrI, 0.01–0.85), IMRT (OR, 0.13; 95% CrI, 0.01–0.72), and IOeRT (OR, 0.25; 95% CrI, 0.04–0.78) showed statistically significant improvements. Since evidence supporting cosmetic outcomes is limited, findings should be interpreted with caution. Among patients with early-stage BC, HF-WBI was associated with the lowest rate of postoperative ipsilateral recurrence, whereas CF-WBI was associated with the second-lowest rate. In terms of cosmetic outcomes, 3D-CRT and IMRT demonstrated favorable clinical efficacy. Additional randomized controlled trials are necessary to clarify the comparative advantages and limitations of CF-WBI, HF-WBI, 3D-CRT, and IMRT, thereby strengthening the evidence base for early-stage BC radiotherapy strategies.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/, identifier CRD420251173161.

Background: Ethylmalonic encephalopathy 1 (ETHE1), a persulfide dioxygenase, is abnormally expressed in various malignancies, but its mechanism and therapeutic potential in lung cancer remain unclear. This study aimed to elucidate the molecular mechanisms through which ETHE1 promotes lung cancer progression via coordination of the PI3K/AKT signaling pathway and tumor metabolism. The feasibility of using ETHE1 as a therapeutic target was also explored. Methods: Bioinformatics analysis was used to assess ETHE1 expression levels in lung cancer tissues and its relationship with patient prognosis. ETHE1-overexpressing and ETHE1-silenced lung cancer cell models were constructed. CCK-8, BrdU, and Transwell assays were used to detect cell proliferation, migration, and invasion capabilities. Nude mouse lung metastasis models were established to validate the functions of ETHE1 in vivo. Western blotting was used to analyze the activation status of the PI3K/AKT signaling pathway. Coexpression analysis and functional enrichment analysis were performed to explore the mechanisms underlying the effects of ETHE1. Molecular docking and cellular experiments were employed to screen potential ETHE1 inhibitors and evaluate their antitumor effects. Results: ETHE1 was significantly overexpressed in human lung cancer tissues and closely associated with poor patient prognosis. Functional enrichment analysis revealed that genes coexpressed with ETHE1 were involved mainly in cellular metabolism and signal transduction processes. In vitro and in vivo experiments confirmed that ETHE1 overexpression significantly promoted lung cancer cell proliferation, migration, invasion, and lung metastasis. Mechanistic studies revealed that ETHE1 exerted oncogenic effects by activating the PI3K/AKT signaling pathway. ETHE1 forms a regulatory axis with the key metabolic enzyme hexokinase 2 (HK2), further amplifying its oncogenic effects. ETHE1 silencing significantly enhanced lung cancer cell sensitivity to chemotherapy drugs such as cisplatin and partially reversed drug resistance. Drug screening identified neobavaisoflavone (NBIF) as an effective ETHE1 inhibitor. NBIF treatment suppressed ETHE1 expression and enhanced chemotherapy sensitivity. Conclusion: ETHE1 plays a crucial role in lung cancer progression by activating the PI3K/AKT signaling pathway and regulating HK2-mediated metabolism. ETHE1 silencing or NBIF inhibition significantly suppressed malignant tumor behaviors and enhanced chemotherapy sensitivity. These findings establish ETHE1 as a promising therapeutic target for lung cancer treatment.

Gastric cancer remains one of the most common malignant tumors worldwide and is associated with a high disease burden. Its treatment is still challenged by multidrug resistance, an immunosuppressive tumor microenvironment, and suboptimal postoperative recovery. Traditional Chinese Medicine (TCM) has shown potential in the prevention, treatment, and rehabilitation of gastric cancer. Herein, this review aims to discuss the basic theory, clinical practice, technical progress, epidemiological research, controversies and challenges, and future prospects of TCM in gastric cancer treatment. Literature from the past five years was retrieved from PubMed and China National Knowledge Infrastructure (CNKI) using English and Chinese search terms related to gastric cancer, TCM, Chinese herbal medicine, integrated traditional Chinese and Western medicine, clinical outcomes, mechanisms, network pharmacology, metabolomics, immunotherapy, chemotherapy resistance, postoperative recovery, and translational research. Experimental studies, clinical studies, cohort studies, randomized trials, meta-analyses, guideline-related studies, and technical studies were considered only if they were relevant to the scope of this narrative review. Based on these, we discuss how TCM may exert potential anti-gastric cancer effects through the regulation of apoptotic pathways, modulation of signaling networks, and improvement of immune function. Currently, clinical studies indicate that TCM combined with chemotherapy may prolong survival in patients with advanced gastric cancer, while perioperative interventions such as transcutaneous electrical acupoint stimulation and herbal formulations may alleviate postoperative pain, promote gastrointestinal recovery, and regulate inflammatory responses. Technological advances such as network pharmacology, metabolomics, and nano-preparation technologies have been used to help clarify the molecular mechanisms of TCM and improve drug delivery efficiency. In addition, observational and real-world evidence suggest that TCM use is associated with survival-related outcomes, patient acceptance, and regional differences in clinical application patterns. Despite these findings, challenges remain, including insufficient high-quality clinical evidence, lack of standardization in syndrome differentiation and efficacy evaluation, and the need for more rigorous safety assessment. Overall, TCM may serve as a complementary component of integrated gastric cancer management, particularly in supportive care, postoperative recovery, and treatment tolerance, but its clinical value remains dependent on the quality of supporting evidence. Future studies should use standardized protocols, rigorous clinical designs, reproducible quality-control systems, and appropriate safety assessment to define its role within modern precision oncology.

Ovarian cancer remains one of the most lethal gynecologic malignancies due to its asymptomatic onset and the lack of reliable early stage diagnostic tools. Immunosensor technologies have emerged as powerful platforms capable of detecting ovarian cancer-associated biomarkers with high sensitivity, specificity, and rapid turnaround times. Recent advances in nanomaterials, microfluidic integration, and signal amplification strategies have significantly enhanced the analytical performance of electrochemical, optical, and piezoelectric immunosensors. These innovations enable ultrasensitive quantification of key biomarkers such as CA 125, HE4, mesothelin, and emerging multi marker panels, supporting earlier detection and improved disease monitoring. Furthermore, the development of portable and point of care immunosensing devices offers promising avenues for decentralized screening and personalized clinical decision making. This review highlights the latest technological breakthroughs, design principles, and translational challenges in immunosensor based ovarian cancer diagnostics, emphasizing their potential to transform early detection and patient outcomes.

Intracavitary perfusion with bevacizumab plus cisplatin shows more clinical benefits versus cisplatin alone in lung cancer patients with malignant pleural effusion (MPE), while there lacks a comprehensive assessment. This meta-analysis reviewed data from randomized controlled trials (RCTs) to comprehensively evaluate the efficacy and safety of intracavitary perfusion with bevacizumab plus cisplatin in these patients. Cochrane Library, Web of Science, PubMed, Wanfang, CNKI, and VIP databases were used for study searching until July 2024. Total efficacy rate (defined as complete response and partial response), pleural fluid vascular endothelial growth factor (VEGF) after treatment, and adverse reactions were analyzed. Twenty RCT studies involving 1316 patients were included. Elevated total efficacy rate [relative risk (RR) (95

Extracellular adenosine has recently been identified as an immunological checkpoint mediator that hinders the immune response to malignancies. The production of adenosine is facilitated by the enzymatic activity of CD39 and CD73. There is an increasing body of evidence suggesting that CD39 and CD73, which are considered to be emerging immunological checkpoints, can transform adenosine triphosphate (ATP)-mediated pro-inflammatory tumor microenvironment (TME) into an adenosine-mediated immunosuppressive through purinergic pathway. The aim of this study was to review macrophages-based cancer immunotherapy by adenosinergic CD39 and CD73 as emerging immune checkpoints. We searched the PubMed, EMBASE, Web of Science, and Medline (Ovid) databases to find relevant studies between December 30, 2010, and December 30, 2024. The search strategy encompassed utilization of Cancer, Immune checkpoints, CD39, CD73, Immunotherapy as keywords. The case reports, reviews, evaluations, originals, and earlier meta-analyses were all included in the study. The inclusion criteria were the researches that investigated the functions of the adenosinergic immunological checkpoints CD39 and CD73 in cancer immunotherapy. Clinical studies have examined small molecule inhibitors or monoclonal antibodies that target the CD39/CD73 pathway in recent years. Cancer immunotherapy might profit from therapeutic inhibition of CD39 and CD73’s enzymatic activity, given that these two proteins are crucial for the conversion of ATP into adenosine. Multiple types of monoclonal antibodies have been developed and shown to inhibit CD39 or CD73. One benefit of using monoclonal antibodies to block CD39 and CD73 is that antibody medications usually have lengthy serum half-lives. Inhibiting CD39 and CD73 may contribute to limiting the progression of tumors and boost anti-tumor responses. Currently, one of the most promising strategies in immuno-oncology is to target CD39 and CD73 due to their extensive immune regulatory effects on tumor immunity.

Lactylation, a recently identified histone modification derived from lactate metabolism, has emerged as a critical regulator of epigenetic reprogramming, tumor proliferation, and immune evasion. In ovarian cancer, lactate dehydrogenase A (LDHA) and other metabolic enzymes contribute to lactate accumulation, which supports chemotherapy resistance and disease progression. Although lactylation is increasingly linked to therapy failure, its precise molecular connection with ovarian cancer, as well as its therapeutic potential are unclear. Traditional analytical approaches often fail to integrate the complexity of multi-omics, limiting the discovery of actionable lactylation-associated vulnerabilities. This research aims to develop an AI-driven multi-omics framework to identify lactylation-related genes, stratify patient drug responses, and establish prognostic signatures in ovarian cancer. Transcriptomic, epigenomic, pharmacogenomic, mutation, and clinical outcome data were collected from The Cancer Genome Atlas (TCGA), the Genomics of Drug Sensitivity in Cancer (GDSC), and independent ovarian cancer cohorts. Deep learning models, including variational autoencoders (VAEs), Long Short-Term Memory (LSTM) networks, and Multitask Multilayer Perceptrons (MLPs) (LSTM-MLP), were applied for molecular subtyping, survival analysis, and IC50 prediction. Findings were validated through pathway enrichment, mutation mapping, immune infiltration profiling, and structure-guided drug repurposing, the proposed method achieved precision of (0.955). Key lactylation-related genes, including LDHA and SLC16A3, were associated with immune exhaustion and cisplatin resistance. The Gln-TEx score and lactylation risk signature robustly predicted patient survival and drug response across TCGA and validation cohorts. Perturbation sensitivity and repurposing analyses revealed novel therapeutic vulnerabilities. This study establishes a precision oncology framework that integrates lactylation biology with AI-driven analytics to uncover druggable targets, enhance patient stratification, and inform the design of multi-target therapies in ovarian cancer.

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide, with high morbidity and occurrence. Although various therapeutic approaches have been rapidly developed in recent years, the underlying molecular mechanisms in the pathogenesis of HCC remain enigmatic. The N6-methyladenosine (m6A) RNA modification is believed to regulate RNA metabolism and further gene expression. This process is intricately regulated by multiple regulators, such as methylases and demethylases. Non-coding RNAs (ncRNAs) are involved in the regulation of the epigenetic modification, mRNA transcription and other biological processes, exhibiting crucial roles in tumor occurrence and development. The m6A-ncRNA interaction has been implicated in the malignant phenotypes of HCC and plays an important role in drug resistance. This review summarizes the effect of m6A-ncRNA crosstalk on HCC progression and their clinical implications as prognostic markers and therapeutic targets in this disease.

The identification of biomarkers correlated with colorectal cancer (CRC) prognosis holds substantial importance from both clinical and scientific perspectives. Zinc finger protein 26 (ZNF26) has not been previously investigated or documented in solid tumors; thus, further research is necessary to ascertain its prognostic value in CRC. Gene expression profiles and clinicopathological data were acquired from The Cancer Genome Atlas (TCGA) database. Subsequently, expression correlation was assessed utilizing the TCGA CRC cohort. The prognostic value of ZNF26 was evaluated through Kaplan-Meier (KM) and ROC curve analyses. Following this, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were conducted to perform enrichment analysis between high- and low-ZNF26 expression groups. The association between immune cells, immune checkpoint genes, and ZNF26 expression levels was examined. Lastly, the research findings were further validated using CRC tissue samples. The results revealed that, in comparison to healthy controls, CRC significantly reduced ZNF26 expression. Elevated ZNF26 expression was associated with poorer overall survival in CRC patients. Additionally, high ZNF26 expression exhibited an inverse relationship with the immunological score and immune checkpoint gene expression in CRC patients. The findings from the TCGA data analysis were corroborated by the PCR results obtained from CRC tissue samples. ZNF26 is markedly upregulated in colorectal cancer tissues, potentially serving as a biomarker for CRC.

BACKGROUND:This study aims to investigate centrosomal protein 70 (CEP70) in prostate cancer and its effects on angiogenesis and tumour metastasis and elucidate its molecular mechanisms. METHODS:We evaluated CEP70 and Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) in tissue samples from patients with prostate cancer by immunohistochemistry. In vitro experiments included overexpressing CEP70 through transfection and assessing its impact on human umbilical vein endothelial cells (HUVECs). Intervention experiments with an NF-κB pathway inhibitor were conducted to verify the mechanism. Finally, the effects of CEP70 on tumour growth, angiogenesis and metastasis were examined in a nude mouse model. RESULTS:CEP70 was significantly overexpressed in prostate cancer tissues compared with that in adjacent normal tissues (p < 0.001). In vitro experiments demonstrated that CEP70 overexpression promoted HUVEC migration (p < 0.001), invasion (p < 0.001) and tube formation (p < 0.05). CEP70 significantly upregulated VEGFA expression in prostate cancer cells at messenger RNA (mRNA) (p < 0.001) and protein levels (p < 0.05). VEGFA knockdown experiments confirmed CEP70 as an essential cytokine for CEP70-induced angiogenesis (p < 0.01). Mechanistically, CEP70 promoted VEGFA expression by activating the NF-κB signalling pathway, as evidenced by the reversal of CEP70-induced effects upon treatment with the NF-κB inhibitor BAY11-7082 (p < 0.01). CONCLUSIONS:CEP70 promotes tumour angiogenesis and metastasis by upregulating VEGFA through NF-κB pathway activation.

Background: Treating glioma with triptolide (TP) produces unsatisfactory outcomes. Previous studies showed that TP combined with succinic acid could sustain antitumor activity during cancer treatment. However, this activity of TP linked with succinic acid has been less investigated during the treatment of glioma. In this study, triptolide-succinic acid ester was synthesized, and its antitumor activity in glioma cells in vitro was determined.Methods: TP was coupled with succinic anhydride (SA) to obtain triptolide-succinic acid ester (TP-SAE). Cell counting kit-8 (CCK-8), transwell, wound healing assays, and flow cytometry analysis of apoptosis were used to evaluate the antitumor activity of TP-SAE in vitro.Results: Results from the cell counting kit-8 assay revealed that TP-SAE rapidly reduced proliferation of glioma cells compared with TP and TP + SA. Transwell and wound healing assays revealed that TP-SAE significantly decreased the invasion and migration of glioma cells compared with TP and TP + SA. The flow cytometry apoptosis assay indicated that apoptosis in glioma cells treated with TP-SAE was significantly higher than in those treated with TP and TP + SA. Conclusions: Triptolide-succinic acid ester could inhibit the proliferation, invasion, and migration activity of glioma cells and promote apoptosis of glioma cells in vitro.

Objective Autophagy is the catabolic process where the components of eukaryotes experience damage, and the affected or superfluous components undergo self-degradation. However autophagy can promote cancer cell apoptosis or facilitate cell growth. This work aimed to investigat the significance of autophagy-related genes (ARGs) in predicting the prognosis of breast cancer (BC) intervened with Cremastra. Methods Active ingredients and action targets were obtained using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and SwissTargetPrediction. Then, the BC transcriptome and clinical data were downloaded in The Cancer Genome Atlas (TCGA), whereas ARGs were collected in the Human Autophagy Database (HADb). Meanwhile, Perl and R software were used for data processing and analysis. Firstly, the transcriptome data of BC were mapped to ARGs to screen the BC-ARGs. Secondly, the above genes were mapped to the action targets of Cremastra, ARGs of Cremastra-intervened BC were then screened out. Moreover, an enrichment analysis of biological function was carried out. Univariate Cox regression was carried out on ARGs of BC for preliminarily selecting the independent prognostic genes and constructing the autophagy prognosis model. These genes were mapped to ARGs involved in Cremastra-intervened BC. Finally, those mapped genes were optimized by multi-factor Cox regression, and the key ARGs and potential compounds were obtained. Finally, all cases were classified as low- or high-risk group based on the median risk score. Receiver operating characteristic (ROC) curve, Kaplan-Meier (K-M) survival, independent prognosis and clinical correlation analyses were conducted for model evaluation and identification of factors to independently predict prognosis. Results Altogether, 66 active components and 38 targets of the Cremastra-intervened autophagy of BC were screened and the autophagy prognosis model demonstrate good predictive performance. As suggested by the survival curve, low-risk patients had a markedly increased survival rate compared with high-risk patients (P < .01). Besides, the gene expression levels of the high-risk group increased with the increases in patients' risk scores. Upon univariate regression, 34 differentially expressed ARGs related to BC treatment were screened. Multivariate regression identified 4 key ARGs, which were mainly derived from glycosides, lignans, flavonoids, and dibenzyl compounds. Thereafter, key genes were subjected to correlation analysis between clinicopathological features and prognosis, among which BCL2 and TP63, showed independent prognostic value. Conclusions In this study, an autophagy prognosis model was established, and BCL2 and TP63 were predicted for the Cremastra intervention of BC by Bioinformatics, which will be applied to further work.

Objective:The efficacy of different external treatment methods of traditional Chinese medicine in the treatment of cancer-related fatigue was analyzed by using network meta-analysis.Methods:Searches were conducted on PubMed, China Journal Full-text Database, Embase platform and so on. Filter according to the inclusion and exclusion criteria, and obtain the network relationship diagram through stata15.0 analysis.Results:This study included 31 articles and 6 kinds of external treatment of traditional Chinese medicine. The results showed that the Piper's fatigue scale(PFS) score improvement was ranked as follows: transcutaneous electrical acupoint stimulation+ conventional treatment > auricular point sticking+ conventional treatment > acupuncture+ moxibustion+ conventional treatment > acupuncture+ conventional treatment > acupoint application+ conventional treatment > moxibustion+ conventional treatment > conventional treatment. Significant differences were also observed between traditional Chinese medicine external treatment combined with conventional treatment and conventional treatment ( P<0.05). The results showed that the Karnofsky performance status(KPS) score improvement was ranked as follows: acupuncture+ moxibustion+ conventional treatment > acupuncture+ conventional treatment > moxibustion+ conventional treatment > acupoint application+ conventional treatment > auricular point sticking+ conventional treatment > conventional treatment. Among them, the top three intervention measures had statistically significant differences compared with conventional treatment ( P<0.05). Conclusion:External treatment of traditional Chinese medicine has a significant effect on improving cancer-related fatigue symptoms. However, due to the small sample size of this study, the results obtained in PFS and KPS scores are inconsistent, and the conclusion needs further confirmation.

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.

Cisplatin (DDP) based chemotherapy occurs a reduced therapeutic effect on the later treatment of ovarian cancer (OC) due to DDP resistance. Astragaloside II (ASII), a natural product extracted from Radix Astragali, has shown promising anticancer effects. However, the effects of ASII on OC have not been clarified. In this study, we found that ASII inhibited cell growth and promoted cell apoptosis of DDP-resistant OC cells in vitro and in vivo. Further study showed that ASII downregulated multidrug resistance-related protein MDR1 and cell cycle-related protein Cyclin D1 and PCNA, and also upregulated apoptosis-related protein leaved PRAP and cleaved caspase-3. In addition, ASII induced autophagy, characterized by upregulation of LC3II expression, downregulation of p62 expression, and elevation of LC3 punctuation, may be associated with inhibition of the AKT/mTOR signaling pathway. Moreover, the messenger RNA-sequencing was used to identify potential molecules regulated by ASII. In conclusion, these findings indicated that ASII increased sensitivity of DDP in the treatment of OC.

胃为传送水谷之通道,以通为用,以降为顺,喜润而恶燥,凡能疏调气机,恢复胃腑和顺通降职能之法皆为通法,通法蕴含虚实平允、寒热平调、气血平和、阴阳平秘之意.胃癌病机为本虚标实,本虚为脾胃虚弱,标实为癌毒留滞,本质是"不通".初期气血瘀滞、痰凝互结,以标实为主;后期则正气虚馁,以本虚为主.应在健脾助运,补益后天的基础上,佐以清热解毒、理气活血、化痰散结、燥湿坚阴等法.健脾补虚用四君子汤、补中益气汤等;湿热蕴结脾胃用藤梨根、无花果、薏苡仁、黄连温胆汤、苍术、黄连、苦参等;平调寒热用半夏泻心汤;气虚血瘀者加补气活血化瘀药物;病程后期,加益气养阴药物.

Colorectal cancer is a common clinical malignant tumor of the digestive tract, and intestinal flora has played an important role in the development of colorectal cancer. Bifidobacteria, as one of the main dominant florae in intestinal tract, can inhibit the occurrence and development of colorectal cancer through various mechanisms. Recent studies have shown that traditional Chinese medicine can regulate the abundance of bifidobacteria in intestinal tract and exhibit anti-tumor effects on colorectal cancer. Detailed investigations have revealed that the mechanisms of bifidobacteria in the treatment of colorectal cancer involve three aspects: the production of short-chain fatty acids, the regulation of the body's immunity, and the regulation of cell apoptosis and differentiation. In this review, we provide an updated summary of recent advances in our understanding of the mechanisms by which traditional Chinese medicine regulate intestinal flora to inhibit colorectal cancer development and metastasis.

Stomach adenocarcinoma (STAD) is a common gastric histological cancer type with a high mortality rate. Immunogenic cell death (ICD) plays a key factor during carcinogenesis progress, whereas the prognostic value and role of ICD-related genes (ICDRGs) in STAD remain unclear. The MSigDB database collecting ICDRGs were selected by univariate Cox regression analysis and LASSO algorithm to establish a novel risk model. The Kaplan-Meier survival analysis indicated a significant difference of OS rate of patients by risk score stratification. ESTIMATE, CIBERSORT, and single sample gene set enrichment analysis (ssGSEA) algorithms were conducted to estimate the immune infiltration landscape by risk stratification. Subgroup analysis and tumor mutation burden analysis were also analyzed to identify characteristics between groups. Differences in therapeutic responsiveness to chemotherapeutic drugs and targeted drugs were also analyzed between high-risk group and low-risk group. The impact of one ICDRG, GPX1, on the proliferation, migration and invasiveness of was confirmed by in vitro experiments in GC cells to test the reliability of bioinformatics results. This study gives evidence of the involvement of ICD process in STAD and provides a new perspective for further accurate assessment of prognosis and therapeutic efficacy in STAD patients. Stomach adenocarcinoma (STAD) is a common gastric histological cancer type with a high mortality rate. Immunogenic cell death (ICD) plays a key factor during carcinogenesis progress, whereas the prognostic value and role of ICD-related genes (ICDRGs) in STAD remains unclear. The MSigDB database collected ICDRGs were selected by univariate Cox regression analysis and LASSO algorithm to establish a novel risk model. The Kaplan-Meier survival analysis indicated a significant difference of OS rate of patients by risk score stratification. ESTIMATE, CIBERSORT, and single sample gene set enrichment analysis (ssGSEA) algorithms were conducted to estimate the immune infiltration landscape by risk stratification. Subgroup analysis and tumor mutation burden analysis were also analyzed to identify characteristics between groups. Differences in therapeutic responsiveness to chemotherapeutic drugs and targeted drugs were also analyzed between high-risk group and low-risk group. The impact of one ICDRG, GPX1, on the proliferation, migration and invasiveness of was confirmed by in vitro experiments in GC cells to test the reliability of bioinformatics results. This study gives evidence of the involvement of ICD process in STAD and provides a new perspective for further accurate assessment of prognosis and therapeutic efficacy in STAD patients.

Immune effector cells in the microenvironment tend to be depleted or remodeled, unable to perform normal functions, and even promote the malignant characterization of tumors, resulting in the formation of immunosuppressive microenvironments. The strategy of reversing immunosuppressive microenvironment has been widely used to enhance the tumor immunotherapy effect. Signal transducer and activator of transcription 3 (STAT3) was found to be a crucial regulator of immunosuppressive microenvironment formation and activation as well as a factor, stimulating tumor cell proliferation, survival, invasiveness and metastasis. Therefore, regulating the immune microenvironment by targeting the STAT3 oncogenic pathway might be a new cancer therapy strategy. This review discusses the pleiotropic effects of STAT3 on immune cell populations that are critical for tumorigenesis, and introduces the novel strategies targeting STAT3 oncogenic pathway for cancer immunotherapy. Lastly, we summarize the conventional drugs used in new STAT3-targeting anti-tumor applications.