As one of the most common malignant tumors， digestive system tumors exhibit an increase in the incidence and mortality year by year. Its pathogenesis is complex， making it difficult to carry out early prevention. Autophagy is a process in which cells use lysosomes to degrade their organelles and macromolecules to maintain cellular homeostasis under the regulation of autophagy-related genes. Cellular autophagy has a dual regulatory effect on the tumor microenvironment， which always affects the occurrence and development of digestive system tumors. Therefore， the effect and mechanism of action of cellular autophagy on digestive system tumors have become a hot topic in tumor therapy in recent years. Meanwhile， the remarkable research results of targeted autophagy drugs indicate that cellular autophagy may become an important target for anti-digestive system tumors. Traditional Chinese medicine （TCM） has been widely used in the comprehensive treatment of digestive system tumors with good efficacy. A variety of active ingredients in TCM， such as flavonoids， glycosides， terpenoids， quinones， and alkaloids， can increase the expression of autophagy-associated proteins microtubule-associated protein 1 light chain 3 （LC3）Ⅱ/Ⅰ， autophagy-related gene （ATG）5， ATG7， inhibit the expression of autophagy-related protein p62 ， and induce autophagy in digestive system tumor cells， thereby exerting the anti-digestive system tumor effect. By summarizing the research results in recent years on the modulation of cell autophagy by active ingredients in TCM to fight against digestive system tumors， this paper analyzed the relevant signaling pathways， regulatory factors， and functional characteristics of cell autophagy modulation， so as to elucidate the mechanism by which active ingredients of TCM induce autophagy and to provide ideas and references for clinical application.

As one of the most common malignant tumors， digestive system tumors exhibit an increase in the incidence and mortality year by year. Its pathogenesis is complex， making it difficult to carry out early prevention. Autophagy is a process in which cells use lysosomes to degrade their organelles and macromolecules to maintain cellular homeostasis under the regulation of autophagy-related genes. Cellular autophagy has a dual regulatory effect on the tumor microenvironment， which always affects the occurrence and development of digestive system tumors. Therefore， the effect and mechanism of action of cellular autophagy on digestive system tumors have become a hot topic in tumor therapy in recent years. Meanwhile， the remarkable research results of targeted autophagy drugs indicate that cellular autophagy may become an important target for anti-digestive system tumors. Traditional Chinese medicine （TCM） has been widely used in the comprehensive treatment of digestive system tumors with good efficacy. A variety of active ingredients in TCM， such as flavonoids， glycosides， terpenoids， quinones， and alkaloids， can increase the expression of autophagy-associated proteins microtubule-associated protein 1 light chain 3 （LC3）Ⅱ/Ⅰ， autophagy-related gene （ATG）5， ATG7， inhibit the expression of autophagy-related protein p62 ， and induce autophagy in digestive system tumor cells， thereby exerting the anti-digestive system tumor effect. By summarizing the research results in recent years on the modulation of cell autophagy by active ingredients in TCM to fight against digestive system tumors， this paper analyzed the relevant signaling pathways， regulatory factors， and functional characteristics of cell autophagy modulation， so as to elucidate the mechanism by which active ingredients of TCM induce autophagy and to provide ideas and references for clinical application.

Breast cancer （BC）， a common malignant tumor in women， is characterized by high incidence and mortality rates， posing a serious threat to women's life and health. Currently， the commonly used treatments for BC include surgery， radiotherapy， chemotherapy， molecular targeted therapy， and endocrine therapy. Although radiotherapy and chemotherapy can effectively kill tumor cells and inhibit the proliferation and differentiation of tumor cells， they can induce adverse reactions such as hematopoietic dysfunction and impaired immune function. The other treatment methods also have problems such as drug resistance， high recurrence rates， reduced quality of life， and poor clinical efficacy. Therefore， it is urgent to explore new drugs with better efficacy and lower toxicity. Ferroptosis is a form of iron-dependent， non-apoptotic programmed cell death triggered by lipid peroxidation. In recent years， ferroptosis has become a hot topic in the field of cancer treatment and has been gradually proven to effectively inhibit the proliferation and metastasis of BC cells， reduce the drug resistance of BC to chemotherapy drugs， and enhance the sensitivity of BC to radiotherapy. Traditional Chinese medicine （TCM）， with multiple components， multiple targets， and mild side effects， is widely used in the treatment of BC. A large number of studies have shown that active ingredients of TCM， such as saponins， flavonoids， terpenoids， phenols， and polysaccharides， can inhibit the proliferation and metastasis of BC cells by modulating ferroptosis-related pathways. These include iron metabolism， lipid metabolism， cystine/glutamate antiporter system Xc^-/glutathione/glutathione peroxidase 4， Specifically， these ingredients elevate the levels of lipid peroxidation， reactive oxygen species， malondialdehyde， and Fe²⁺ in BC cells， thereby inducing ferroptosis-mediated suppression of tumor progression. This article reviews the relevant literature at home and abroad in recent years， summarizes the mechanisms of ferroptosis in regulating BC and the research progress in the active components of TCM targeting ferroptosis in the intervention of BC， aiming to provide ideas for the development of new drugs for the treatment of BC.

BACKGROUND: The available evidence regarding the benefits of percutaneous coronary intervention (PCI) on patients receiving dialysis with coronary artery disease (CAD) is limited and inconsistent. This study aimed to evaluate the association between PCI and clinical outcomes as compared with medical therapy alone in patients undergoing dialysis with CAD in China. METHODS: This multicenter, retrospective study was conducted in 30 tertiary medical centers across 12 provinces in China from January 2015 to June 2021 to include patients on dialysis with CAD. The primary outcome was major adverse cardiovascular events (MACE), defined as a composite of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke. Secondary outcomes included all-cause death, the individual components of MACE, and Bleeding Academic Research Consortium criteria types 2, 3, or 5 bleeding. Multivariable Cox proportional hazard models were used to assess the association between PCI and outcomes. Inverse probability of treatment weighting (IPTW) and propensity score matching (PSM) were performed to account for potential between-group differences. RESULTS: Of the 1146 patients on dialysis with significant CAD, 821 (71.6%) underwent PCI. After a median follow-up of 23.0 months, PCI was associated with a 43.0% significantly lower risk for MACE (33.9% [ n  = 278] vs . 43.7% [ n  = 142]; adjusted hazards ratio 0.57, 95% confidence interval 0.45-0.71), along with a slightly increased risk for bleeding outcomes that did not reach statistical significance (11.1% vs . 8.3%; adjusted hazards ratio 1.31, 95% confidence interval, 0.82-2.11). Furthermore, PCI was associated with a significant reduction in all-cause and cardiovascular mortalities. Subgroup analysis did not modify the association of PCI with patient outcomes. These primary findings were consistent across IPTW, PSM, and competing risk analyses. CONCLUSION This study indicated that PCI in patients on dialysis with CAD was significantly associated with lower MACE and mortality when comparing with those with medical therapy alone, albeit with a slightly increased risk for bleeding events that did not reach statistical significance.
Humans ; Percutaneous Coronary Intervention/methods* ; Male ; Female ; Coronary Artery Disease/drug therapy* ; Retrospective Studies ; Renal Dialysis/methods* ; Middle Aged ; Aged ; China ; Proportional Hazards Models ; Treatment Outcome

With the increasing utilization of cancer therapy, the incidence of lung injury associated with these treatments continues to rise. The recognition of pulmonary toxicity related to cancer therapy has become increasingly critical, for which interstitial lung disease (ILD) is a common cause of mortality. Cancer therapy-related ILD (CT-ILD) can result from a variety of treatments including chemotherapy, targeted therapy, immune checkpoint inhibitors, antibody-drug conjugates, and radiotherapy. CT-ILD may progress rapidly and even be life-threatening; therefore, prompt diagnosis and timely treatment are crucial for effective management. This review aims to provide valuable information on the risk factors associated with CT-ILD; elucidate its underlying mechanisms; discuss its clinical features, imaging, and histological manifestations; and emphasize the clinical-related views of its diagnosis. In addition, this review provides an overview of grading, typing, and staging treatment strategies used for the management of CT-ILD.
Humans ; Lung Diseases, Interstitial/diagnosis* ; Neoplasms/therapy* ; Risk Factors ; Immune Checkpoint Inhibitors/adverse effects* ; Antineoplastic Agents/therapeutic use*

As a common malignant tumor of the respiratory system， the incidence and mortality of lung cancer are still rising year by year. Its pathogenesis is complex， the prognosis is poor， and it seriously affects human physical and mental health. Although existing Western medical treatments can inhibit tumor growth to a certain extent and relieve patients' painful symptoms， problems such as postoperative recurrence and metastasis， numerous adverse reactions， and the tendency to develop drug resistance make the overall therapeutic effect unsatisfactory. Therefore， it is urgent to seek more efficient and safer treatments. Adenosine monophosphate-activated protein kinase （AMPK） signaling pathway can regulate the growth， differentiation， apoptosis， and autophagy of lung cancer cells， and is extensively involved in the occurrence and development of lung cancer， thus being regarded as an important target for anti-lung cancer therapy. Traditional Chinese medicine （TCM） exerts anti-lung cancer effects through multiple pathways， mechanisms， and targets， with advantages such as preventing postoperative recurrence and metastasis， alleviating the adverse reactions of radiotherapy and chemotherapy， and improving quality of life. TCM has therefore become a key approach in current anti-lung cancer treatment. Studies have found that active components of Chinese medicine， including flavonoids， saponins， polyphenols， and terpenes， as well as Chinese medicine compound prescriptions such as Guiqi Yiyuan extract， Qingzao Jiufei decoction， and Yiqi Fuzheng formula， have significant regulatory effects on AMPK and its interacting signaling pathways. These effects include inducing autophagy and apoptosis of lung cancer cells， modulating macrophage polarization， inhibiting epithelial-mesenchymal transition， reversing drug resistance， and blocking the cell cycle， thereby exerting anti-lung cancer activity. This article reviews and summarizes recent studies on the anti-lung cancer effects of TCM， and discusses the mechanisms by which TCM regulates the AMPK signaling pathway in the treatment of lung cancer， with the aim of providing ideas and references for the development of new clinical anti-lung cancer drugs.

As a common malignant tumor of the respiratory system， the incidence and mortality of lung cancer are still rising year by year. Its pathogenesis is complex， the prognosis is poor， and it seriously affects human physical and mental health. Although existing Western medical treatments can inhibit tumor growth to a certain extent and relieve patients' painful symptoms， problems such as postoperative recurrence and metastasis， numerous adverse reactions， and the tendency to develop drug resistance make the overall therapeutic effect unsatisfactory. Therefore， it is urgent to seek more efficient and safer treatments. Adenosine monophosphate-activated protein kinase （AMPK） signaling pathway can regulate the growth， differentiation， apoptosis， and autophagy of lung cancer cells， and is extensively involved in the occurrence and development of lung cancer， thus being regarded as an important target for anti-lung cancer therapy. Traditional Chinese medicine （TCM） exerts anti-lung cancer effects through multiple pathways， mechanisms， and targets， with advantages such as preventing postoperative recurrence and metastasis， alleviating the adverse reactions of radiotherapy and chemotherapy， and improving quality of life. TCM has therefore become a key approach in current anti-lung cancer treatment. Studies have found that active components of Chinese medicine， including flavonoids， saponins， polyphenols， and terpenes， as well as Chinese medicine compound prescriptions such as Guiqi Yiyuan extract， Qingzao Jiufei decoction， and Yiqi Fuzheng formula， have significant regulatory effects on AMPK and its interacting signaling pathways. These effects include inducing autophagy and apoptosis of lung cancer cells， modulating macrophage polarization， inhibiting epithelial-mesenchymal transition， reversing drug resistance， and blocking the cell cycle， thereby exerting anti-lung cancer activity. This article reviews and summarizes recent studies on the anti-lung cancer effects of TCM， and discusses the mechanisms by which TCM regulates the AMPK signaling pathway in the treatment of lung cancer， with the aim of providing ideas and references for the development of new clinical anti-lung cancer drugs.

Gastrointestinal tumors （GTs）， including colorectal cancer， gastric cancer， liver cancer， pancreatic cancer， and esophageal cancer， are increasing in incidence worldwide and have become one of the major diseases threatening human health. Tumor stem cells （TSCs）， an undifferentiated subpopulation within tumor tissues， possess biological characteristics such as self-renewal， multidirectional differentiation， high tumorigenicity， and resistance to radiochemotherapy. They play an important role in the occurrence， progression， recurrence， and metastasis of GTs and have increasingly become a research hotspot in GT treatment. Although modern medicine has made remarkable progress， there remain many problems in therapeutic approaches targeting TSCs. In this context， traditional Chinese medicine （TCM）， with its favorable safety profile and multi-target mechanisms， has shown potential advantages and value in regulating TSCs. It can reduce TSC drug resistance， enhance the sensitivity of tumor cells to chemotherapeutic agents， inhibit tumor growth and metastasis， and has shown unique advantages in improving the quality of life and prolonging the survival of GT patients. Studies have found that active components of Chinese medicine， such as terpenoids， polyphenols， flavonoids， glycosides， and quinones， and Chinese medicine compound formulas， including Zuojin pills， Sijunzi decoction， Biejiajian pills， and Xuanfu Daizhe decoction， can inhibit TSCs-related signaling pathways such as the Notch signaling pathway， the Wnt/β-catenin signaling pathway， the phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） signaling pathway， and the Hippo signaling pathway. They also reduce the expression of TSC surface markers， including sex-determining region Y-box 2 （SOX2）， sex-determining region Y-box 9 （SOX9）， octamer-binding transcription factor 4 （OCT4）， prominin-1 （CD133）， cluster of differentiation 44 （CD44）， cluster of differentiation 24 （CD24）， and thyroid transmembrane protein 1 （CD90）， thereby hindering TSC differentiation， accelerating their metabolic processes， improving the tumor microenvironment， and consequently inhibiting GT growth. This study collects and analyzes recent research on the regulation of TSCs by TCM in the treatment of GT， aiming to provide a new theoretical basis for tumor therapy with TCM， expand its application in the comprehensive treatment of GT， and offer new therapeutic ideas and methods for clinical practice.

Objective:To investigate the relationship between the radioresistance of anaplastic thyroid cancer (ATC) and the induction of epithelial-mesenchymal transition (EMT).Methods:Firstly, the radiotherapy sensitivity of differentiated thyroid cancer cells (TPC-1, FTC-133) and ATC cells (CAL-62, 8305C), and the protein levels of E-cadherin, N-cadherin and vimentin proteins after 6 Gy irradiation were detected. The changes in transcriptional levels before and after 4 Gy X-ray radiation of ATC cells were analyzed using mRNA sequencing. Then, the ATC radio-resistant cell models were constructed and validated, and the cell line with the highest radio-resistance was selected for subsequent experiments. Radio-resistant cells were classified into the control group (no treatment), EMT-inhibitor group (EMT-inhibitor-1 pre-treatment), Vactosertib group [transforming growth factor-β(TGF-β) inhibitor Vactosertib pre-treatment), and si-Snail group (knockdown of Snail gene by siRNA transfection), respectively. The expression level of EMT related proteins and TGF-β/Smad signaling pathway related proteins, the cloning efficiency, and the phosphorylated-histone H2A family member X (γH2AX) positive cells rate in the treatment groups and the control group were detected by Western blotting, clone formation assay, immunofluorescence, respectively, reflecting the changes in EMT level and DNA repair ability. Comparison between two groups was performed by Dunnett t-test. Comparison among multiple groups was conducted by one-way ANOVA. Results:The radiosensitivity of ATC cells were lower than that of differentiated thyroid cancer cells. After irradiation, the expression level of E-cadherin was low, those of N-cadherin and vimentin were high, EMT level was increased, and the expression levels of TGF-β/Smad signaling pathway-associated proteins were up-regulated in ATC cells. After use of EMT inhibitor, Vactosertib and Snail knockdown, the expression levels of EMT-associated proteins were down-regulated, cell survival fraction was declined, γH2AX positive cell rate was increased, DNA damage repair ability was weakened and the radiosensitivity was enhanced in radiotherapy-resistant ATC strains. Conclusions:The level of radiotherapy resistance in ATC cells is positively correlated with the EMT level, and the mechanism of radiotherapy resistance is related to the activation of the TGF-β/Smad/Snail pathway after irradiation.

Objective:To explore the predictive value of changes in prealbumin for the prognosis of patients with hepatitis B virus-associated acute-on-chronic liver failure (HBV-ACLF) after artificial liver treatment.Methods:From January 1, 2018 to December 31, 2021, the clinical data (including prealbumin, platelet count, lymphocyte count, alanine transaminase (ALT), etc.) of 87 patients with HBV-ACLF who received artificial liver treatment at the Department of Gastroenterology of the General Hospital of Western Theater Command PLA were retrospectively collected. The 90-day survival status of all the patients was followed up, and the patients were divided into the survival group and the mortality group according to the survival status. The clinical characteristics and the changes of prealbumin on day 1 to 3, day 3 to 7, and day 1 to 7 after artificial liver treatment were compared between the 2 groups. Multivariate logistic regression analysis was used to analyze the independent influencing factors of the 90-day prognosis of HBV-ACLF patients after artificial liver treatment, and the nomogram prediction model was established and the receiver operating characteristic curve (ROC) was drawn to assess the area under the curve (AUC). Hosmer-Lemeshow goodness-of-fit test, calibration curve and clinical decision curve were performed to evaluate the goodness of fit, consistency and clinical value of the prediction model. Paired t-test and Mann-Whitney U test were used for statistical analysis. Results:There were 69 cases enrolled into the survival group, and 18 cases enrolled into the mortality group. The levels of albumin, prealbumin, platelet count, lymphocyte count, and ALT before treatment, and the level of prealbumin at the 3rd day after treatment of the survival group were all higher than those of the mortality group (32.5 (30.6, 35.2) g/L vs. 29.4 (27.6, 32.3) g/L, 66.0 (52.5, 81.5) mg/L vs. 56.5 (39.2, 65.0) mg/L, 103.0 (72.5, 145.0)×10 9/L vs. 63.5 (40.0, 92.5)×10 9/L, 1.1 (0.8, 1.4)×10 9/L vs. 0.9 (0.5, 1.1)×10 9/L, (514.7±86.4) U/L vs. (328.2±93.4) U/L, 90.0 (69.5, 102.5) mg/L vs.68.5(60.0, 75.8) mg/L), and the age, the level of total bilirubin, international normalized ratio, and prothrombin time before treatment of the survival group were all lower than those of the mortality group (48.0 (42.0, 57.0) years old vs. 48.5 (47.0, 56.0) years old, 323.9 (261.2, 409.2) μmol/L vs. 452.2 (405.8, 510.8) μmol/L, 1.5 (1.3, 1.9) vs. 1.9 (1.4, 2.1), 17.3 (14.6, 20.8) s vs. 21.4 (16.6, 23.2) s), and the differences were statistically significant ( Z=-3.38, -2.87, -2.38 and -2.01, t=2.39, Z=-4.11, 3.00, 3.64, 2.18 and 2.37; all P<0.05). The change of prealbumin on day 1 to 3 after treatment in the mortality group was greater than that in the survival group (-0.182 (-0.321, -0.026) vs. -0.043 (-0.133, 0.093)), and the difference was statistically significant ( Z=-3.42, P=0.001). The results of multivariate logistic regression analysis showed that the age, total bilirubin before treatment, and the change of prealbumin on day 1 to 3 after treatment were independent influencing factors for the 90-day prognosis in HBV-ACLF patients after artificial liver treatment (all P<0.05), and the nomogram model was established based on the above 3 factors. The results of ROC analysis showed that the AUC of the prediction model was 0.933 (95% confidence interval: 0.866 to 1.000, P<0.001), with a sensitivity of 0.933 and a specificity of 0.825. The results of the Hosmer-Lemeshow goodness-of-fit test showed that the prediction model had a good fit( P=0.700). The results of calibration curve analysis indicated that the actual curve of the prediction model was close to the calibration curve, with an average absolute error of 0.034, the consistency between the predicted probability and the actual probability was good. The clinical decision curve analysis suggested that the prediction model had significant clinical benefits. Conclusions:The changes of prealbumin after artificial liver treatment in HBV-ACLF patients can reflect the recovery of liver function. The nomogram prediction model based on the change of prealbumin on day 1 to 3 after treatment, age, and total bilirubin before treatment can better predict the 90-day prognosis of HBV-ACLF patients after artificial liver treatment.