OBJECTIVE:This study investigated the effects of Shenling Baizhu decoction (SLBZD) on chemotherapy-induced sarcopenia and its potential mechanisms. METHODS:A mouse model of chemotherapy-induced sarcopenia was established and treated with SLBZD. The effects of SLBZD on body weight, food intake, muscle mass, muscle functional markers, muscle tissue architecture, and serum biochemical parameters in mice receiving chemotherapy were determined, and the potential mechanism was investigated. RESULTS:The study indicated that SLBZD effectively alleviated chemotherapy-induced weight loss and decreased food intake, muscle atrophy, and functional loss in mice. It increased the CSA level, decreased the serum IFN-γ, IL-1β, and TNF-α levels, increased ATP content and IGF-1 protein expression in muscle tissue, and down-regulated MSTN expression. SLBZD down-regulated the mRNA expressions of NLRP3, p65, Caspase-1, and MuRF1 and up-regulated the expression of MyoD. The mechanism is that SLBZD activated PPARγ, inhibited NF-κB phosphorylation, and suppressed NLRP3 inflammasome activation. Transcriptome analysis revealed the regulation of immune-inflammatory pathways and metabolic pathways. Additionally, SLBZD promoted myotube formation and diameter, regulated MuRF1/MyoD, and inhibited NLRP3/NF-κB signaling, effects that could be reversed by a PPARγ inhibitor. DISCUSSION:The findings suggest that SLBZD can prevent sarcopenia by activating PPARγ to inhibit NF-κB/NLRP3 and restore metabolic homeostasis, thereby making it a promising adjunctive therapeutic regimen. CONCLUSION:This study identifies SLBZD as a promising therapeutic agent for chemotherapy- induced sarcopenia, whose functions may be attributed to PPARγ-mediated regulation of inflammatory and metabolic pathways.

BACKGROUND:Immune checkpoint inhibitors elicit responses in merely 20-40% of patients with microsatellite instability-high or mismatch repair-deficient colorectal cancer (CRC), making immunotherapy resistance a formidable clinical challenge. The immunosuppressive tumor microenvironment, characterized by regulatory T-cell accumulation and metabolic reprogramming, substantially drives this treatment failure. PURPOSE:To determine whether neferine, a bioactive alkaloid derived from the traditional Chinese medicine formulation Shenling Baizhu Tang (SLBZT), enhances anti-PD-1 (aPD-1) efficacy in CRC liver metastasis by modulating the CYP2E1-PPARα metabolic axis. METHODS:A CRC liver metastasis model was established via intrasplenic injection of MC38-Luc cells into C57BL/6 J mice. The animals were administered aPD-1 alone or in combination with low- or high-dose SLBZT. Tumor burden was evaluated via in vivo imaging and histopathology. Integrated transcriptomics and metabolomics, CRISPR-Cas9-mediated CYP2E1 knockout, T-cell coculture assays, alongside computational and biophysical analyses, were employed to elucidate the active components and underlying mechanisms. Evaluated functional outcomes included tumor burden, immune phenotyping, CYP2E1/PPARα signaling, and homovanillic acid (HVA) levels. RESULTS:High-dose SLBZT markedly augmented aPD-1-mediated suppression of CRC liver metastasis without compromising systemic tolerability. Multi-omics profiling coupled with genetic validation revealed that CYP2E1-driven lipid metabolic reprogramming and its downstream metabolite HVA serve as key mediators of regulatory T-cell expansion and CD8⁺ T-cell exhaustion. Both SLBZT and neferine diminished HVA accumulation, restored effector T-cell function, and potentiated aPD-1 efficacy. Furthermore, biophysical and computational analyses confirmed the direct inhibition of CYP2E1 by neferine. CONCLUSION:Neferine sensitizes tumors to PD-1 blockade by reprogramming lipid metabolism and remodeling the immune microenvironment via the CYP2E1-PPARα axis, highlighting its translational potential as a metabolic immunoadjuvant to overcome immunotherapy resistance in CRC.

Oxidized low-density lipoprotein (oxLDL) exhibits differential expression in microsatellite-stable (MSS) and microsatellite instability-high (MSI) colorectal cancer (CRC), highlighting its potential therapeutic role in immune checkpoint inhibitor (ICI) resistance in MSS CRC. Elevated oxLDL levels in MSS CRC contribute to tumor progression and diminish ICI efficacy by modulating metabolic reprogramming and immunosuppressive mechanisms within the tumor microenvironment (TME) by activating receptors such as LOX-1 and CD36. oxLDL triggers signaling pathways, including NF-κB, PI3K/Akt, and MAPK, leading to the expansion of immunosuppressive cells like regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and M2 macrophages, while concurrently suppressing effector T cell functions. Additionally, oxLDL enhances oxidative stress and promotes fatty acid oxidation (FAO) and glycolytic metabolism, resulting in nutrient competition within the TME and establishing an immunosuppressive milieu, ultimately culminating in ICI resistance. This review systematically examines the disparities in oxLDL expression between MSS and MSI CRC and elucidates the molecular mechanisms through which oxLDL mediates ICI resistance. Furthermore, it explores potential therapeutic strategies targeting oxLDL, offering novel avenues to overcome immunotherapy resistance in MSS CRC.

ObjectiveTo develop and validate a nomogram for predicting the risk of postoperative prolonged ileus (PPOI) in patients undergoing gastric cancer (GC) surgery, providing a personalized risk assessment tool for early identification and optimized postoperative management.MethodsA retrospective cohort (January 2019-December 2023) was used to develop and internally test the nomogram, while a prospective cohort (January-December 2024) was used for external validation. Univariate and multivariate logistic regression with backward stepwise selection identified independent predictors. Model performance was assessed through receiver operating characteristic (ROC) curves, calibration curves, decision-curve analysis (DCA), and clinical impact curve analysis (CICA). Patients were stratified into low, medium, and high-risk groups based on nomogram scores for further analysis.ResultsA total of 780 patients in the training cohort and 294 in the validation cohort were included, with postoperative prolonged ileus rates of 11.54% and 16.33%, respectively (χ2 = 4.371, P =.037). Independent predictors included electroacupuncture, pain self-efficacy questionnaire (PSEQ) score, preoperative serum albumin (Alb), body fat, postoperative day 1 Visual Analog Scale (Pod1 VAS), and intensive care unit (ICU) admission. The nomogram demonstrated strong discriminatory ability and calibration, with clinical utility confirmed through DCA and CICA. Higher nomogram scores correlated with increased PPOI incidence.ConclusionsThe developed nomogram is a valuable tool for early identification of PPOI in GC patients, supporting clinicians and nurses in implementing personalized preventive strategies.

Traditional Chinese medicine (TCM) Yi-Fei-Jie-Du-Tang (YFJDT) has shown potential in lung cancer treatment. However, the mechanisms underlying the effects of YFJDT on lung cancer remain unclear. Bioinformatics analysis is conducted to identify potential targets of YFJDT. The impact of YFJDT on hypoxia-inducible factor 1 alpha (HIF1A), ferroptosis, and vasculogenic mimicry (VM) is investigated using xenograft tumor models and A549 cells. Additionally, A549 cells are stimulated with CoCl2 to mimic the hypoxic microenvironment of the tumor. The role of HIF1A overexpression in modulating ferroptosis is assessed. The effects of HIF1A and ferroptosis on epithelial-mesenchymal transition (EMT) and VM in vitro are evaluated. Results: YFJDT treatment led to a concentration-dependent decrease in HIF1A levels in xenograft tumors and A549 cells. Overexpression of HIF1A counteractes the inhibitory effects of YFJDT on proliferation, EMT, and VM in transplanted tumors. Moreover, HIF1A overexpression attenuates YFJDT-induced lipid peroxidation and iron accumulation, indicating inhibition of ferroptosis in A549 cells. Hypoxia-induced alterations in EMT markers and VM are reversed by YFJDT but exacerbated by HIF1A overexpression. Molecular docking identified salicylic acid and psoralen as potential components of YFJDT targeting HIF1A. YFJDT exerts anti-tumor effects in lung cancer by downregulating HIF1A and promoting ferroptosis.

Background:Metastatic non-small-cell lung cancer (NSCLC) represents a significant clinical challenge and is the leading cause of cancer-related death worldwide. Immune checkpoint inhibitors (ICIs), particularly those targeting the programmed cell death protein 1 (PD-1)/programmed cell death-ligand 1 (PD-L1) pathway, have transformed the treatment of advanced-stage NSCLC; however, their efficacy varies, and optimal strategies following initial ICI failure remain undefined. Envafolimab, a novel humanized single-domain anti-PD-L1 antibody fragment fused to an Fc domain, is the first globally approved subcutaneous PD-L1 inhibitor. Its unique structure confers advantages in terms of tissue penetration and distribution compared to conventional monoclonal antibodies. Case Description:This report details the case of a 66-year-old male diagnosed with stage IVB (cT4N2M1c) squamous cell carcinoma of the left upper lung with confirmed hepatic metastasis. Initial immunohistochemistry revealed a tumor proportion score for PD-L1 ≥1%, prompting the following standard first-line therapy as per the guidelines: three cycles of albumin-bound paclitaxel [470 mg, day (d)1], carboplatin (568 mg, d1), and pembrolizumab (200 mg, d1). This regimen yielded inadequate disease control. Subsequently, second-line therapy comprising two cycles of gemcitabine (1.6 g, d1; 1.4 g, d8), cisplatin (40 mg, d1-3), endostar (30 mg, d1-4), and subcutaneous envafolimab (200 mg, d1) was initiated. Follow-up computed tomography (CT) imaging revealed a notable reduction in the left hilar mass and significant alleviation of the bronchial obstruction. This therapeutic response was sustained for over 6 months during envafolimab monotherapy maintenance without recurrence. Conclusions:This case shows the potential efficacy of envafolimab-based combination therapy in achieving a clinically significant and durable response for a patient with metastatic squamous NSCLC (sq-NSCLC) who showed disease progression on first-line pembrolizumab-containing chemotherapy. It suggests that envafolimab warrants consideration as a viable treatment option in this setting, particularly following the failure of PD-1 inhibitors. Further larger clinical trials need to be conducted to confirm these findings and define its optimal role in the NSCLC treatment sequence.

OBJECTIVE:To investigate the benefits of Traditional Chinese Medicine (TCM) therapy for improving the survival of patients with stage I gastric cancer (GC) and high-risk factors in a real-world setting. METHODS:The clinical data of patients who were diagnosed with stage I GC from March 1, 2012 to October 31, 2020 were collected. Prognostic analysis was performed to explore the high-risk factors that affected the survival of the patients. A Cox multivariate regression model was used to compare the hazard ratios for the mortality risk of patients, especially those with high-risk factors. Kaplan-Meier survival curve and log-rank test were utilized to assess the survival time. RESULTS:Prognostic analysis demonstrated that female sex, tumor invasion into blood vessels, and Ib stage were independent risk factors. The 1-, 3-, and 5-year survival rates of the TCM group those of the non-TCM group were 100.0% 91.0%, 97.6% 64.5%, and 81.4% 55.5%, respectively. A significant difference in median overall survival (mOS) was found between the two groups (χ = 7.670, = 0.006). Subgroup analysis showed that the mOS of female patients and stage Ib patients in the TCM group were longer than those in the non-TCM group ( ≤ 0.001 and 0.001, respectively). CONCLUSIONS:TCM treatment can improve the survival of patients with stage I GC and high-risk factors.

ETHNOPHARMACOLOGICAL RELEVANCE:The traditional Chinese medicine herb Celastrus orbiculatus Thunb. is an important folk medicinal plant in China that has been used as an anti-inflammatory, antitumor, and analgesic in various diseases. Recent years, many studies have reported the significant effects of Celastrus orbiculatus Thunb. extract (COE) on gastric cancer. However, the specific mechanism by which COE regulates gastric cancer cytoskeleton remodeling and thus inhibits EMT has not yet been reported.AIM OF STUDY:To study the effect and mechanism of COE in inhibiting the epithelial-mesenchymal transition (EMT) and metastasis of gastric cancer cells, laying an experimental foundation for the clinical application and further development of COE.METHODS:The high-content cell dynamic tracking system was used to continuously track the trajectory of cell movement in real time. Through the high-content data, the average movement distance and movement speed of the cells are calculated. Additionally, the dynamic images of the cell movement in the high-content imaging system are derived to analyze the impact of COE on the movement of gastric cancer cells. Cytoskeleton staining experiment was performed to detect the effect of COE on the assembly of gastric cancer cell cytoskeleton proteins. Western blot was employed to detect the changes of EMT and metastasis-related proteins in the gastric cancer cells treated by COE. The effect of COE on the key regulatory protein Cofilin-1 (CFL1) of cell movement was examined by Western blot and protein degradation experiment. The effect of COE on EMT and metastasis of the gastric cancer cells lacking CFL1 was assessed by a transwell assay. The in vivo inhibitory effect of COE on EMT and metastasis of gastric cancer was determined by the animal living image system. IHC assays were used to detect the levels of EMT-related proteins in COE reversal in vivo.RESULT:The results showed that the movement distance and average movement speed of gastric cancer cells after COE treatment were significantly lower than those of the control group. Cytoskeleton staining experiments revealed that COE can significantly change the distribution of skeletal proteins in gastric cancer cells. Additionally, COE treatment significantly reduced the expression of Matrix metalloproteinases (MMP-2, MMP-9) and other proteins. Furthermore, COE can significantly accelerate the degradation of CFL1 protein, and both COE treatment and CFL1 deletion can significantly inhibit EMT and metastasis of gastric cancer cells. Lastly, the number of peritoneal metastases of gastric cancer cells was significantly reduced in animals after COE treatment. COE can reverse the levels of EMT-related proteins while reducing the expression levels of CFL1 protein in vivo.CONCLUSION:COE can significantly inhibit EMT and metastasis of gastric cancer cells in vivo and in vitro. This effect may be achieved by reducing the stability of CFL1 and inhibiting the assembly of actin in gastric cancer cells.

Background:Signal transducers and activators of transcription (STAT) proteins, well-known cytoplasmic transcription factors, were found to be abnormally expressed in various cancers and play essential parts in the initiation, progression and therapy resistance of cancer. Nevertheless, the functions of different STATs in pancreatic cancer (PC) and their relationship to the prognosis and immune infiltration as well as drug efficacy in PC patients have not been systematically elucidated.Methods:Expression, prognosis, genetic alterations and pathway enrichment analyses of the STAT family were investigated via Oncomine, GEPIA, Kaplan Meier-plotter, cBioPortal, Metascape and GSEA. Analysis of tumor immune microenvironment was conducted by ESTIMATE and TIMER. "pRRophetic" packages were used for analysis of chemotherapeutic response. Finally, the diagnostic and prognostic value of key STATs were further validated through public datasets and immunohistochemistry.Results:In this study, only STAT1 mRNA level was significantly increased in tumor tissues and highly expressed in PC cell lines via multiple datasets. PC patients with higher STAT1/4/6 expression had a worse overall survival (OS) and progression-free survival (PFS), while higher STAT5B expression was correlated with better prognosis in the TCGA cohort. The STATs-associated genes were enriched in pathways about the remodeling of tumor immune microenvironment. The STATs levels were significantly correlated with immune infiltration, except STAT6. The STAT1 was identified as a potential biomarker and its diagnostic and prognostic value were further validated at mRNA and protein levels. GSEA showed that STAT1 may be involved in the progression and immune regulations of PC. Moreover, STAT1 expression was significantly related to the level of immune checkpoint, and predicted immunotherapy and chemotherapy responses.Conclusion:STAT family members were comprehensively analyzed and STAT1 was identified as an effective biomarker for predicting the survival and therapeutic response, which could be beneficial to develop better treatment strategies.

Long non-coding RNA (lncRNA) contains rich information and functions. The research on Traditional Chinese Medicine (TCM) targeting lncRNA mainly involves tumors, cardiovascular diseases, endocrine and metabolic related diseases, osteoporosis and other diseases, which are used to explore the mechanism of TCM and the differetiation of TCM syndromes or constitution, etc. LncRNA has important application prospects in the field of TCM. The study of lncRNA may provide new ways and technical methods for the research of modern TCM.

目的:分析扶正清毒方联合SOX化疗方案治疗晚期胃癌的临床疗效.方法:90例晚期胃癌患者按照随机数字表法分为治疗组和对照组,每组各45例.对照组给予SOX化疗方案,治疗组在对照组治疗基础上给予扶正清毒方.比较两组患者无进展生存期(progress free survival,PFS)、生活质量、临床疗效、中医证候评分及不良反应.结果:治疗过程中,对照组脱落3例、治疗组脱落2例,故最终完成试验85例.治疗组中位PFS为16.8个月,对照组中位PFS为9.7个月,两组PFS比较,差异有统计学意义(P＜0.05).治疗后,治疗组患者卡氏评分明显高于治疗前,且高于同期对照组卡氏评分(P＜0.05).治疗组疾病控制率为88.37％(38/43),对照组疾病控制率为66.67％(28/42),两组疾病控制率比较,差异有统计学意义(x2=5.767,P＜0.05).治疗后,治疗组患者的中医证候评分显著低于治疗前,且低于同期对照组(P＜0.05).治疗组、对照组贫血发生率分别为25.58％(11/43)、47.62％(20/42),血小板减少发生率分别为9.30％(4/43)、28.57％(12/42),恶心呕吐发生率分别为9.30％(4/43)、33.33％(14/42);两组化疗后贫血、血小板减少及恶心呕吐发生率比较,差异均有统计学意义(P＜0.05).结论:扶正清毒方联合SOX化疗方案治疗晚期胃癌临床疗效显著,可以延长患者的PFS,改善患者临床症状,提高生活质量,降低不良反应(贫血、血小板减少、恶心呕吐)发生率.

1 健脾养血浓煎剂 组 成:生黄芪60 g,炒白术20 g,女贞子40 g,墨旱莲40 g,黄精30 g,灵芝40 g,花生衣60 g,石韦20 g,阿胶30 g,生地黄40 g,当归20 g,白芍60 g,鸡血藤40 g,焦山楂20 g,竹茹30 g,法半夏20 g,炙甘草6 g.

Background: Poria cocos (P. cocos) is an important medicinal fungus in traditional Chinese medicine. Poria acid (PA), a triterpenoid compound, is an effective component of traditional Chinese medicine P. cocos. This experiment investigated the anti-gastric cancer biological activity of PA in vitro. Methods: The effect of PA on the viability of gastric cancer cells was detected by the thiazolyl blue (MTT) assay. Cell adhesion assays were used to detect changes in the adhesion of cells treated after PA (0, 20, 40, and 80 µmol/L). The ability of cell invasion and migration were detected by Transwell assays and wound healing assays. A high-content imaging system was used to dynamically record the motility of the gastric cancer cells after PA (0, 20, 40, and 80 µmol/L) treatment. Western blotting was used to detect the expression of epithelial–mesenchymal transformation (EMT), invasion and migration related proteins. Results: The MTT assay showed that the proliferation of gastric cancer cells was significantly inhibited after PA treatment. Cell adhesion experiments showed that the adhesion of gastric cancer cells was significantly decreased after PA treatment. Compared with the control group, the wound healing area of the gastric cancer cells treated with different concentrations of PA decreased. The Transwell assay showed that the number of gastric cancer cells passing through the cell membrane were significantly reduced after PA treatment. In addition, after PA treatment, the cells’ movement distance and average movement speed were significantly lower than those of the control group. Finally, PA can significantly alter the expression of EMT-related proteins E-cadherin, N-cadherin, and Vimentin and decreased the expressions of metastasis-related proteins matrix metalloproteinase (MMP) 2, MMP-9 and tissue inhibition of matrix metalloproteinase (TIMP)1 in the gastric cancer cells. Conclusions: Triterpenoids from P. cocos have significant biological activity against gastric cancer, and the mechanism may be involved in the process of epithelial–mesenchymal transformation.

BACKGROUND Gastric cancer is the fifth most common tumor and has the third-highest mortality rate among various malignant tumors, and the survival rate of patients is low. Celastrus orbiculatus extract (COE) has been shown to inhibit the activity of a variety of tumors. In this study, we examined the inhibition of the epithelial-mesenchymal transition (EMT) process in gastric cancer cells by COE through the transforming growth factor-β(TGF-β) signaling pathway. METHODS COE was first diluted to various concentrations and then used to treat SGC-7901, BGC-823, MGC-803, and AGS cells. Cell proliferation was assessed by an MTT (thiazole blue) assay. Transwell assays were used to assess cell invasion and migration. The high-content imaging technology was used to further observe the effects of the drug on cell invasion and migration. Western blotting was used to assess the effects of the drug on the expression of EMT and Smad2/3 signaling pathway-related proteins. RESULTS We found that COE inhibited the migration and invasion of AGS gastric cancer cells in a dose-dependent manner. Consequently, COE decreased the expression of EMT-related proteins and proteins related to the Smad2/3 signaling pathway in gastric cancer cells, inhibiting the migration and invasion of gastric cancer cells, and this effect occurred through the TGF-β signaling pathway. SUMMARY We investigated that COE could inhibit the proliferation of gastric cancer cells and inhibit invasion and metastasis by inhibiting the EMT process at the molecular level and its effect on the TGF-β signaling pathway.

Yi-Fei-Jie-Du-Tang (YFJDT) is a traditional Chinese medicine formulation. Our previous studies have demonstrated that YFJDT can be used to treat non-small-cell lung cancer (NSCLC), but its protective effect against NSCLC and its mechanisms remain unclear. In the present study, we evaluated the protective effects and potential mechanisms of YFJDT on a tumor-bearing mouse lung cancer model and A549 cell model. Tumor-bearing mice and A549 cells were treated with YFJDT, tumors were measured during the experiment, and tumor tissues and cell supernatants were collected at the end of the experiment to assess the levels of autophagy and epithelial-mesenchymal transition (EMT)-related proteins. The results showed that YFJDT treatment reduced tumor volume and mass, increased the expression of the autophagy marker LC3, and inhibited EMT-related proteins compared with the model group. Cell survival was reduced in the YFJDT-treated groups compared with the model group, and YFJDT also reduced the migration and invasion ability of A549 cells in a dose-dependent manner. Western blotting detected that YFJDT also upregulated FAT4 in the tumor tissue and A549 cells and downregulated the expression of vimentin. Meanwhile, apoptosis in both tissues and cells was greatly increased with treatment of YFJDT. We further interfered with FAT4 expression in cells and found that the inhibitory effect of YFJDT on EMT was reversed, indicating that YFJDT affects EMT by regulating FAT4 expression. Taken together, results of this study suggested that the inhibitory effect of YFJDT on EMT in lung cancer tumors is through upregulating FAT4, promoting autophagy, and thus inhibiting EMT in cancer cells.

The presence of the blood-brain barrier (BBB) remains a challenge in the treatment of central nervous system (CNS) diseases, as it hinders the infiltration of many therapeutic drugs into the brain parenchyma. Therefore, developing efficacious pharmacological agents that can traverse the BBB is crucial for optimal treatment of diseases of the CNS such as neurodegenerative conditions and brain tumors. Adeno-associated virus (AAV), one of the most promising gene therapy vectors, has been shown to cross the BBB safely and is non-pathogenic in nature and therefore has been utilized for numerous diseases of the CNS. Along with the development of protein engineering techniques such as directed evolution including DNA shuffling, a great number of BBB-crossing AAVs have been developed, that could be systemically injected for therapeutic benefit. In this review, we discuss several feasible approaches to improve transportation of therapeutic agents to the CNS. We also discuss the advantages of using BBB-crossing AAVs, their role as a gene delivery agent and highlight the different types of BBB-AAV vectors that have been developed in order to provide a greater insight into how they can be used in diseases of the CNS.

Objective . This meta-analysis was conducted to compare the therapeutic efficacy and clinical safety of the combination therapy of apatinib plus chemotherapy with that of chemotherapy alone in patients with refractory or recurrent ovarian carcinoma (OC). Methods . Relevant randomized controlled trials (RCT) or case-control studies (CCS) were identified by searching Chinese and English databases up to October 31, 2020. The risk of methodological bias tool and Newcastle–Ottawa scale (NOS) were used to assess trial quality. Pooled odds ratios (OR) and 95% confidence intervals (CI) were calculated to evaluate the therapeutic effects and adverse drug reactions. Subgroup analyses of study type, study sample size, dosage of apatinib, and chemotherapy regimen between treatment group and control group were performed. Publication bias was assessed by funnel plot symmetry, Begg–Mazumdar test, and Egger test. The robustness of our results was presented by removing the trial one by one. Results . Fifteen eligible studies covering 1,020 patients were included in this review and meta-analysis. Among these studies, 8 were RCTs, and 7 were CCSs. Compared with chemotherapy alone, apatinib plus chemotherapy significantly increased objective response rate (OR = 3.55; 95% CI 2.31 to 5.47), disease control rate (OR = 3.04; 95% CI 2.12 to 4.36), and overall survival (OR = 5.03; 95% CI 3.16 to 6.90). Conclusions . The combination treatment of apatinib plus chemotherapy provides better clinical benefits for OC patients when compared to chemotherapy alone and should be recommended for suitable patients with OC after the failure of standard regimens. However, further investigation into future large-scale prospective randomized research is still needed.

Glioblastoma multiforme (GBM) is a brain tumor with a high mortality rate. Surgical resection combined with radiotherapy and chemotherapy is the standard treatment for GBM patients, but the 5-year survival rate of patients despite this treatment is low. Immunotherapy has attracted increasing attention in recent years. As the pioneer and the main effector cells of immunotherapy, T cells play a key role in tumor immunotherapy. However, the T cells in GBM microenvironment are inhibited by the highly immunosuppressive environment of GBM, posing huge challenges to T cell-based GBM immunotherapy. This review summarizes the effects of the GBM microenvironment on the infiltration and function of different T-cell subsets and the possible strategies to overcome immunosuppression, and thus enhance the effectiveness of GBM immunotherapy.

Objective To evaluate the therapeutic effect of Traditional Chinese Medicine (TCM), specifically Fuzheng Qingdu (FZQD) therapy, on the survival time of metastatic GC patients. Patients and Methods Databases of medical records of 6 hospitals showed that 432 patients with stage IV GC were enrolled from March 1, 2012 to October 31, 2020. Propensity score matching (PSM) was used to reduce the bias caused by confounding factors in the comparison between the TCM and the non-TCM users. We used a Cox multivariate regression model to compare the hazard ratio (HR) value for mortality risk, and Kaplan-Meier survival curve for the survival time of GC patients Results The same number of subjects from the non-TCM group were matched with 122 TCM-treated patients after PSM to evaluate their overall survival (OS) and progression-free survival (PFS). Median time of OS of TCM and non-TCM users were 16.53 and 9.10 months, respectively. TCM and non-TCM groups demonstrated a 1-year survival rate of 68.5% and 34.5%, 2-year survival rate of 28.6% and 3.5%, and 3-year survival rate of 17.8% and 0.0%, respectively. A statistical difference exists in OS between the 2 groups (χ 2 = 33.39 and P < .0001). The PFS of TCM users was also longer than that of non-TCM users (χ 2 = 4.95 and P = 0.026). Notably, Chinese herbal decoction, Shenmai and compound Kushen injections were commonly used for FZQD therapy. Conclusion This propensity-matched study showed that FZQD therapy could improve the survival of metastatic GC patients.