Objective To summarize the papers about the research status and prospects of ferroptosis in hepatocellular carcinoma (HCC) and its drug resistance in recent years in order to provide directions and ideas for the treatment of HCC. Method The relevant literatures at home and abroad in recent years about ferroptosis in HCC and its drug resistance were reviewed. Results The mechanism of ferroptosis in the development and drug resistance of HCC was complicated, involving multiple protein and molecular pathways. Ferroptosis played an important role in improving chemotherapy and sorafenib resistance, and it had a broad application prospect in HCC. Conclusions The molecular mechanism of ferroptosis in HCC and its drug resistance has not been fully elucidated. Further research on the mechanism of ferroptosis in HCC may provide new molecular therapeutic targets for HCC. Ferroptosis has a broad application prospect in the treatment of HCC.
In recent years, with the wide application of carbapenems, the resistance of Enterobacterium to carbapenems has become increasingly high, leading to a large number of carbapenem-resistant Klebsiella pneumoniae (CRKP). These bacteria are often resistant to many different types of antibacterial drugs, including carbapenems, which leads to clinical treatment failure and seriously threatens the life safety of patients. Currently, these bacteria have become an independent risk factor for patients’ death. This article reviews the drug resistance, infection status and influencing factors, and medication therapy of CRKP, in order to facilitate the clinical diagnosis, treatment, and disease process control of CRKP infection, and provide reference for curbing bacterial drug resistance.
ObjectiveTo systematically elucidate the resistance mechanism of targeted drug therapy for breast cancer and to discuss the future direction of optimized treatment strategies. MethodA literature review on targeted therapy for breast cancer had been conducted based on recent domestic and international researches. ResultsContemporary breast cancer targeted therapies maincomprised human epidermal growth factor receptor 2 (HER2)-directed agents, CDK4/6 inhibitors, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB/AKT) / mechanistic target of rapamycin (mTOR) pathway blockers, poly (ADP-ribose) polymerase inhibitors, and immune checkpoint modulators, etc. While these agents conferred subtype-specific survival benefits, resistance developed through target mutations, compensatory signaling, epigenetic alterations, drug efflux pumps, etc. Emerging reversal drug resistance strategies involved dual-targeted approaches (such as trastuzumab in combination with pertuzumab), dynamic monitoring of drug-resistant gene mutations by liquid biopsy, epigenetic modulators, etc. ConclusionsDrug resistance remains a key bottleneck limiting long-term efficacy of breast cancer targeted therapy. Future research should integrate multi-omics approaches to decipher tumor heterogeneity, implement combinatorial multi-target inhibition with real-time monitoring of multidimensional interventions, and leverage artificial intelligence to predict resistance evolution. This integrated strategy will enable personalized combination therapies, ultimately overcoming drug resistance and improving patient survival outcomes.