To analyze the characteristics of adverse drug reaction (ADR) in a specialized stomatology hospital and thus provide references for clinical rational drug use and risk management.

Ovarian cancer is the most lethal malignancy of the female reproductive system worldwide. Chemoresistance, particularly platinum resistance, is a major factor limiting improvement in prognosis, and its underlying mechanisms involve complex regulation of and escape from multiple programmed cell death pathways in cancer cells. Disulfidptosis is triggered by high expression of solute carrier family 7 member 11 (SLC7A11) under glucose starvation and shares upstream regulatory nodes with ferroptosis. Necrosis by sodium overload is driven by sodium ion overload mediated by transient receptor potential cation channel subfamily M member 4 (TRPM4), but its role remains to be further investigated. Other programmed cell death pathways are interwoven into a dynamic regulatory network through key regulatory molecules such as tumor protein p53, the caspase family, cysteine-aspartic proteases, and glutathione. Autophagy can inhibit pyroptosis; ferroptosis and pyroptosis can synergistically amplify cell-killing effects through the reactive oxygen species/NOD-like receptor thermal protein domain-associated protein 3 axis; ferroptosis and cuproptosis share the glutathione metabolic axis; and the interaction between ferroptosis and disulfidptosis can shift from antagonism to synergy under specific metabolic stress. Ferroptosis and necrosis by sodium overload mutually promote each other through cascades involving adenosine triphosphate depletion, reactive oxygen species accumulation, and mitochondrial damage. PANoptosis can overcome cancer-cell resistance to a single mode of cell death through the simultaneous activation of multiple cell death pathways. A comprehensive review of the roles and interactive networks of various programmed cell death modalities, including disulfidptosis, necrosis by sodium overload, apoptosis, autophagy, necroptosis, pyroptosis, ferroptosis, cuproptosis, and PANoptosis, in platinum resistance in ovarian cancer is expected to provide a solid theoretical basis and potential translational directions for reversing platinum resistance and optimizing clinical treatment strategies.

This study aimed to characterize the somatic variant candidate gene profile of patients with chemotherapy-associated aplastic anemia (CAA) and compare it with that of patients with cancer without aplastic anemia (non-AA) and primary aplastic anemia (PAA). This study included 24 patients with CAA diagnosed at Peking Union Medical College Hospital from September 2019 to May 2023 (male-to-female ratio of 3∶5; median age, 60 years). Peripheral blood samples were collected for whole-exome sequencing, and the results were compared with publicly available data of patients with non-AA and PAA. A total of 37 111 variants across 9 958 genes were detected. KEGG enrichment analysis revealed that these genes were mainly concentrated in the JAK-STAT and calcium signaling pathways (all P<0.01). Regarding human leukocyte antigen (HLA) genes, the mutation frequency of HLA-DRB1 was higher in patients with CAA than in those with non-AA cancer [false discovery rate (FDR) =0.029], whereas the mutation frequencies of HLA-A (FDR=0.082) and HLA-C (FDR=0.058) were lower than in those with PAA. For myeloid disease-related genes, compared with patients with non-AA cancer, those with CAA had higher mutation frequencies in 198 genes, including BRCA2 (FDR=0.032) and ASXL1 (FDR=0.047), and lower frequencies in SAA2 (FDR=0.049), TP53 (FDR=0.045), and PIK3CA (FDR=0.049). Compared with patients with PAA, those with CAA had higher mutation frequencies in 213 genes, including BRCA2 (FDR=0.068) and ATRX (FDR=0.072), and lower frequencies in 14 genes, including ASXL1 (FDR=0.045) and DNMT3A (FDR=0.078). In conclusion, the somatic variant profile of CAA significantly differs from that of non AA cancer and PAA: its degree of immune abnormality is higher than that in non-AA cancer but milder than that in PAA; it shows a higher potential for myeloid evolution than non-AA cancer, but its transformation mechanism is more complex than that of PAA, being influenced by multiple factors including primary tumor characteristics and myeloid gene variants.

Immune checkpoint inhibitors (ICIs) are increasingly used in cancer therapy; however, systematic epidemiological studies of ICI-associated cardiovascular adverse events in China remain limited. This study aims to analyze cardiovascular adverse event signals associated with ICIs approved by the Food and Drug Administration (FDA), thereby providing evidence to support safer clinical use.

To investigate the factors influencing quality of life in patients with chemotherapy-induced peripheral neuropathy (CIPN) and to construct a risk prediction model.

Carrimycin is a macrolide antibiotic widely used in the pharmaceutical and clinical fields， with its primary composition consisting of three distinct derivatives of spiramycin. For decades， macrolides like carrimycin have been valued for their efficacy against Gram-positive bacteria and certain atypical pathogens. However， as research has progressed， recent studies have revealed that carrimycin， along with various other structurally modified spiramycin derivatives， exhibits significant antitumor activity in multiple experimental models. This finding suggests that the spiramycin molecular scaffold possesses intrinsic potential beyond its conventional antibacterial role. By strategically modifying the substituents attached to this core structure， it may be feasible to develop novel compounds with enhanced and more selective antitumor properties. Despite this promising outlook， research into the specific targets and comprehensive mechanisms underlying the antitumor effects of spiramycin derivatives remains notably insufficient. A major gap exists in the precise identification of their molecular targets within cancer cells and the detailed signaling pathways they modulate. This lack of mechanistic understanding poses a substantial barrier to the rational design， optimization， and clinical translation of spiramycin-based antitumor therapeutics. To systematically address this knowledge gap and elucidate the antitumor mechanism of this compound class， the present study adopted an activity-based protein profiling （ABPP） strategy. ABPP is a chemoproteomic approach that enables the direct identification of functionally active proteins that interact with small-molecule probes in a native biological context. As a first step， we designed and synthesized a novel， high-activity spiramycin derivative termed n-hexanoyl spiramycin （h-SPM）. Building upon the structure of h-SPM， we subsequently engineered and synthesized a structurally analogous activity-based probe. This probe was specifically functionalized with chemical handles （such as an alkyne group） compatible with ABPP methodologies， allowing for downstream bioorthogonal conjugation and enrichment steps. The experimental workflow began by incubating this active probe with live cancer cells. During this co-incubation period， the probe engaged with and covalently bound to its potential protein targets within the complex cellular environment. Following the interaction， cells were lysed， and the probe-labeled proteins were efficiently isolated and purified using affinity-based enrichment techniques-specifically via copper-catalyzed azide-alkyne cycloaddition （click chemistry） to immobilize them onto a solid support. The enriched protein pool was then subjected to in-depth analysis using liquid chromatography-mass spectrometry （LC-MS）. This analytical phase yielded detailed， proteome-wide information on the identities of proteins that interact with the h-SPM-based probe. To extract biological insights from the list of identified proteins， we performed comprehensive bioinformatic analysis using Gene Ontology （GO） enrichment. This systematic classification provided crucial information regarding the biological processes， molecular functions， and cellular components associated with the captured proteins. The functional annotations derived from GO analysis allowed us to evaluate and prioritize several promising candidate target proteins for further experimental validation. Through this integrated proteomic and bioinformatic approach， we successfully identified multiple potential cellular targets of h-SPM. Notable among these were amyloid precursor protein （APP） and low-density lipoprotein receptor （LDLR）， both of which are implicated in diverse cellular processes such as cell adhesion， signal transduction， and metabolic regulation. To confirm the biological relevance of these interactions， we employed Western Blotting experiments. These studies verified that the expression or post-translational modification states of APP and LDLR were altered in response to h-SPM treatment， thereby confirming their status as responsive molecular targets. After identifying and preliminarily validating APP as a key interactor， we proceeded to investigate its functional role in the drug's mechanism of action. Using short hairpin RNA （shRNA）-mediated protein knockdown， we generated cancer cell lines with significantly reduced APP expression. Comparative analysis of drug sensitivity between these knockdown cells and their wild-type counterparts revealed a marked attenuation of h-SPM's antitumor effects in the absence of APP. Complementary to this， cell staining assays， including immunofluorescence， were conducted to visualize morphological changes， alterations in cell viability， and the subcellular localization of relevant biomarkers following h-SPM treatment. Collectively， these functional experiments provided compelling evidence that APP plays a critical and indispensable role in mediating the antitumor activity of h-SPM. Our findings thus outline a preliminary model of the drug's mechanism， likely involving cellular pathways regulated or influenced by APP. In summary， this study achieves two significant objectives. First， it establishes and validates a robust， generalizable target-screening platform based on ABPP， specifically tailored for the investigation of spiramycin-class compounds. Second， and more importantly， it delivers novel biological insights by pinpointing specific protein targets such as APP. The identification of these targets provides invaluable mechanistic clues and a solid theoretical foundation for the future development of this family of compounds. This work effectively advances spiramycin derivatives from compounds with observed phenotypic activity toward agents with an emerging mechanistic understanding， thereby paving the way for more targeted drug design and informed combination therapy strategies in oncology. Future studies will focus on delineating the detailed downstream consequences of APP engagement by h-SPM and exploring the therapeutic potential of other identified targets in preclinical models.

Chemotherapy-induced myelosuppression (CIM) is a common and serious adverse reaction during chemotherapy in patients with malignant tumors. Kaempferol, an important active component of leukocyte-elevating traditional Chinese medicine, may play a role in its improvement. This study aims to explore the research status and mechanisms of kaempferol in improving CIM and to provide reference evidence for its application in the prevention and treatment of CIM.

To investigate the incidence of severe cancer therapy-related thrombocytopenia (CTRT) and associated factors in children.

Cisplatin (CDDP) is an anticancer drug widely used in clinical practice. The immunotoxic effects of CDDP residues in the environment on aquatic organisms remain unclear. This study aimed to evaluate the immunotoxic effects of CDDP at environmentally relevant concentrations on zebrafish and to verify the mediating role of the NF-κB signaling pathway. Using zebrafish as a model organism, we systematically investigated the toxicological consequences of CDDP exposure on the immune system. The results showed that CDDP significantly reduced the survival and hatching rates of zebrafish, with a median lethal concentration (LC50) of 0.48 mg/L. In addition, CDDP induced developmental retardation, eye size reduction, and other morphological abnormalities in the larvae, as well as decreased spontaneous locomotion and disrupted light-dark rhythm. In terms of oxidative stress, CDDP exposure elevated reactive oxygen species (ROS) and malondialdehyde (MDA) levels, while decreasing glutathione (GSH) content and catalase (CAT) activity, which indicated impairment of the antioxidant defense system. Immunological analyses revealed abnormal recruitment of macrophages and neutrophils, dysregulated complement C3 levels, and persistent suppression of immunoglobulin M (IgM). Long-term exposure led to altered kidney function markers in adult zebrafish. From a mechanism perspective, CDDP markedly upregulated the expression of key genes in the NF-κB signaling pathway, driving excessive immune-inflammatory responses. These effects were observable even at the environmentally relevant concentration of 0.025 mg/L. This study provides a theoretical basis for elucidating the ecological risks and immunotoxic mechanisms of CDDP in aquatic environments.

This study aimed to explore the impact of dihydroartemisinin (DHA) on cell proliferation, migration, and invasion in oral squamous cell carcinoma (OSCC). Our findings offer a theoretical foundation for advancing the research and development of novel therapeutic agents for OSCC.

To determine whether dentin sialophosphoprotein (DSPP) modulates oxaliplatin efficacy for colorectal cancer (CRC) and explore the underlying integrin αvβ3-dependent mechanism.

To evaluate the associations of serum methotrexate (MTX) concentrations and MTHFR gene polymorphisms with delayed metabolism of high-dose MTX and adverse reactions in children with acute lymphoblastic leukemia (ALL).

Bacterial outer membrane vesicles (OMVs) have attracted widespread attention in the field of drug delivery due to their excellent biocompatibility, tumor penetration, and loading capacity. The anti-angiogenic peptide AP25 can block malignant tumor angiogenesis and has broad-spectrum anti-cancer activity. To achieve efficient delivery of AP25, we modified AP25 on the surface of OMVs through genetic engineering and explored their inhibitory effects on breast cancer and gastric cancer in vitro. The results indicated that the engineered OMVs had typical morphological characteristics of OMVs, and the particle size distribution conformed to the theoretical. Proteinase K digestion combined with Western blotting confirmed that AP25 was modified on the membrane surface of OMVs. Cell experiments showed that WAP25 OMVs significantly inhibited the proliferation, migration, and invasion of MDA-MB-231 and HGC-27 cells, promoted the cell apoptosis, and downregulated the expression of tumor migration and angiogenesis-related proteins: integrin beta 1 (integrin β1), Homo sapiens inhibitor of DNA binding 1 (ID1), nuclear factor kappa-B (NF-κB), and vascular endothelial growth factor (VEGF). This study achieves effective delivery of protein drugs based on OMVs for the first time, providing new ideas for the anti-angiogenesis therapy for tumors and the functional development of bacterial OMVs.

The widespread use of immune checkpoint inhibitors (ICIs) has led to breakthrough advances for patients with various advanced solid tumors. As the skin is an important target organ of immune responses, it is the most commonly affected site of treatment-related adverse events associated with ICIs, with a relatively high incidence of ICI-related skin toxicity events. Immune-related adverse events induced by ICIs are increasingly becoming a bottleneck limiting their clinical application. To collect post-marketing adverse events and medication errors related to drugs and therapeutic biological products and to evaluate real-world drug safety, the United States Food and Drug Administration (FDA) established the FDA Adverse Event Reporting System (FAERS) database. Based on the FAERS database, this study aims to systematically evaluate differences in the risk of skin toxicity events among different drug subtypes, cytotoxic-T-lymphocyte-associated antigen-4 inhibitors, programmed death-1 (PD-1) inhibitors, and programmed death-ligand 1 (PD-L1) inhibitors, and to explore the limitations and potential improvements of existing pharmacovigilance methods.

In recent years, immune checkpoint inhibitors (ICIs), as a revolutionary therapeutic approach in oncology, have demonstrated remarkable clinical efficacy across various malignant tumors. With the widespread clinical application of ICIs, their associated toxicities have emerged as a critical issue that urgently requires resolution in the field of cancer immunotherapy. ICIs-associated pneumonitis (CIP) specifically refers to immune-related adverse events (irAEs) of the lung induced by ICIs therapy, the underlying pathogenesis of which remains incompletely elucidated. As a rare yet severe complication of ICIs treatment, and CIP is characterized by insidious onset, rapid progression, poor prognosis, and high mortality rate, with highly heterogeneous clinical manifestations and radiological features. Due to the lack of specific biomarkers and objective diagnostic indicators, the early identification and diagnosis of CIP present significant clinical challenges. By reviewing previous literature and studies, this paper summarizes recent advances in understanding the clinical manifestations, risk factors, potential molecular mechanisms, biomarkers, and early warning systems of CIP in patients receiving immunotherapy for lung cancer. The aim of this article is to provide a reference for the clinical management of CIP and offer a theoretical basis for establishing an early screening and precision diagnosis and treatment system for this condition.
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To observe the clinical efficacy of heat-sensitive moxibustion in reducing toxicity and enhancing efficacy in cancer patients undergoing chemotherapy, and to provide a scientific basis for its application and promotion in cancer rehabilitation.

To evaluate the inhibitory effect of antitumor component-Ι in Agkistrodon halys venom (AHVAC-I) on proliferation and migration of cisplatin-resistant gastric cancer cells and explore the underlying mechanism.

The ubiquitin-proteasome system (UPS) serves as the central mechanism for protein degradation in eukaryotic cells. Deubiquitinases (DUBs), which maintain protein stability and function by removing ubiquitin chains play a key role in protein cycling. Consequently, a DUB-targeting chimera (DUBTAC) technology has emerged. A DUBTAC consists of three components: a protein-targeting ligand, a DUB recruiter, and a linker connecting them. A DUBTAC can simultaneously bind to its targeted protein and DUB and induce the DUB to cleave the ubiquitin chains, thereby restoring the protein function by stabilizing the target protein. The DUBTAC technology provides a novel research strategy involving targeted protein stabilization for conventionally "undruggable" proteins that are abnormally degraded. Compared with other mature technologies, such as proteolysis-targeting chimera (PROTAC) and molecular glue degrader technologies, the DUBTAC technology has the unique advantages of targeting and stabilizing tumor suppressors, thus showing high potential for cancer therapy. However, it is still in the early stage of development with few systematic summaries of recent research achievements. This review introduces the basic concepts, critical design, and research considerations of DUBTACs, summarizes the latest research advances in DUBTAC technology for antitumor drug development, and discusses the development strategies and clinical application prospects of DUBTACs in the future, aiming to provide more directions for research on this technology.

To investigate the molecular mechanism by which Lichong Xiaozheng Granules (LCXZ) sensitize ovarian cancer to cisplatin (DDP) treatment.

Immune checkpoint blockade (ICB) therapy has demonstrated significant efficacy in the treatment of various cancers. However, a subset of patients develops hyper-progressive disease (HPD) following ICB, which is characterized by accelerated tumor growth and poor clinical outcomes. This review outlines the clinical features, potential mechanisms, and possible intervention strategies of HPD, with the aim of informing clinical practice and providing relevant recommendations.
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