Objective: This study aims to investigate the expression characteristics of GLUT10 in breast cancer and its role in mediating cisplatin resistance, with the goal of providing a new molecular target for personalized breast cancer treatment. Methods: Data from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) databases were analyzed using the GEPIA2 platform to assess pan-cancer expression, while the UALCAN platform was used to analyze expression differences between breast cancer and normal breast tissues. In vitro, SK-BR-3 cells were divided into three groups: shScr (transfected with non-targeting scrambled shRNA), shSLC2A10#1, and shSLC2A10#2. MDA-MB-231 cells were divided into a vector control group and an SLC2A10 overexpression group. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect SLC2A10 mRNA expression. Western blotting was used to detect GLUT10 and cleaved caspase-3 protein expression. The CM-H2DCFDA probe was used to measure intracellular reactive oxygen species (ROS) levels. Drug sensitivity and colony formation assays were performed to evaluate cisplatin sensitivity, and flow cytometry was used to detect apoptosis rates. Results: GEPIA2 analysis showed that GLUT10 expression was downregulated in adrenocortical carcinoma, cervical squamous cell carcinoma and adenocarcinoma, and kidney chromophobe tumor tissues compared to normal tissues, whereas it was upregulated in invasive breast cancer, glioma, skin melanoma, and thymoma. UALCAN analysis revealed that SLC2A10 mRNA levels in breast cancer tissues were 1.85-fold higher than in normal breast tissues (P＜0.001). RT-qPCR results showed that SLC2A10 mRNA expression levels in breast cancer cell lines, ranked from high to low, were Hs 578T (160.5±12.3), SK-BR-3 (115.2±10.5), MDA-MB-468 (50.1±5.2), T-47D (35.4±4.1), and MCF7 (25.6±3.8), all significantly higher than in normal breast epithelial cells (P＜0.001). In SK-BR-3 cells, compared with the shScr group, the shSLC2A10#1 and shSLC2A10#2 groups exhibited increased intracellular ROS levels (relative fluorescence intensity: 1.78±0.12 and 2.05±0.15, respectively; P＜0.05), increased cisplatin sensitivity, reduced colony numbers, and promoted cisplatin-induced ROS accumulation and apoptosis. In MDA-MB-231 cells, compared with the vector control group, the SLC2A10 overexpression group showed decreased intracellular ROS levels (relative fluorescence intensity: 0.58±0.09, P＜0.05), decreased cisplatin sensitivity, and inhibited cisplatin-induced ROS accumulation and apoptosis. Conclusion: GLUT10 is highly expressed in breast cancer and mediates cisplatin resistance by regulating ROS levels, suggesting it may serve as a novel therapeutic target for reversing drug resistance in breast cancer.

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.

Comprehensive chromatographic separation methods were employed to isolate and purify the chemical constituents from the non-alkaloidal fraction of Sophorae Tonkinensis Radix et Rhizoma, and the structures of the compounds were identified with mass spectrometry(MS) and nuclear magnetic resonance(NMR) data. Fourteen prenylated flavonoids were isolated and identified, namely 5-isopentenylsophotonin Ⅰ(1),(2S)-6-isopentenyl-2'-hydroxyglabrol(2), sophoradin(3), sophoradochromene(4), 1-prenylpterocarpin(5), sophoranone(6), glabrol(7), 7,4'-dihydroxy-6,8-diprenyldihydroflavone(8), isobavachin(9), sophoranochromene(10), 5-dehydroxylupinifolin(11), 2-[{2'-(1-hydroxy-1-methylethyl)-7'-(3-methyl-2-butenyl)-2',3'-dihydrobenzofuran}-5'-yl]-7-hydroxy-8-(3-methyl-2-butenyl)chroman-4-one(12), ebenosin(13), and wighteone(14). Among them, compounds 1 and 2 were identified as new compounds, the ~(13)C-NMR data of compounds 3 and 4 were reported for the first time, and compounds 5 and 9 were isolated from this plant for the first time. The MTT assay was used to evaluate the cytotoxic activities of the isolates, and compounds 4, 7, and 10 exhibited significant potent cytotoxic activities on HCT116 cells, with IC_(50) values ranging from 11.44 to 13.43 μmol·L~(-1), comparable with the positive control 5-fluorouracil(5-FU, IC_(50) value is 11.70 μmol·L~(-1)).

The chemical constituents of the ethyl acetate extract from Achyrocline satureioides were rapidly analyzed using ultra performance liquid chromatography-quadrupole time-of-flight tandem mass spectrometry(UPLC-Q-TOF-MS/MS) combined with the Global Natural Products Social Molecular Networking(GNPS) molecular network. The mass spectrometric characteristics of the phloroglucinol compounds were clarified. Guided by these features, systematic isolation was performed using ODS-C_(18), Sephadex LH-20, and semi-preparative high performance liquid chromatography(HPLC). The structures were elucidated using modern spectroscopic techniques such as nuclear magnetic resonance(NMR) spectroscopy and high-resolution mass spectrometry(HR-MS). A total of 38 compounds were identified from the ethyl acetate fraction by mass spectrometry, including 23 flavonoids. Additionally, 18 compounds were isolated from this fraction. Among them, compound 1 was a new unsaturated fatty acid, and compounds 2, 3, and 7-10 were phloroglucinols. Compounds 2, 3, 7, and 8 were obtained from this plant for the first time. The in vitro anti-proliferative activities of compounds 2, 3, and 7-10 against the non-small cell lung cancer cell lines A549 and H1975 were evaluated using the CCK-8 assay. Compound 8 exhibited significant anti-lung cancer activity. This integrated approach using LC-MS/MS combined with GNPS enables efficient analysis of the chemical components in the ethyl acetate fraction of A. satureioides and facilitates the guided isolation of phloroglucinol compounds, thereby enriching the understanding of its material basis.

The incidence and mortality of malignant tumors remain persistently high, while current clinical chemotherapeutic agents are often limited by significant drug resistance and adverse reactions. Consequently, small-molecule compounds derived from traditional Chinese medicine(TCM) have emerged as a focus in anti-tumor research owing to their advantages of multi-targeting action and low toxicity. As the core active component of Glycyrrhiza uralensis, glycyrrhizic acid(GA) is an oleanane-type pentacyclic triterpenoid saponin, constituting 5%-11% of the total content of G. uralensis. Its anti-tumor activity has been validated across various tumor systems, with mechanisms of action encompassing key processes such as cell cycle arrest, induction of tumor cell apoptosis, inhibition of tumor angiogenesis, blockage of invasion and metastasis, regulation of the tumor immune microenvironment(TIME), and alleviation of chronic inflammation. In terms of its therapeutic value, the combination of glycyrrhizic acid with other agents, such as tanshinone Ⅱ_A(Chinese medicine) or cisplatin(conventional chemotherapy) can achieve enhanced efficacy, reduced toxicity, targeted delivery, and reversal of drug resistance. This positions GA as possessing dual values, functioning both as a therapeutic agent and as a drug delivery carrier. This review systematically summarized the anti-tumor pharmacological activities, mechanisms, combined medication potential, and safety profiles of GA. It elaborated on the network mechanism of core regulatory hubs, analyzed the limitations of current research, and proposed targeted strategies for clinical translation. This work aims to provide a reference for the transition of GA from fundamental research to clinical application, while also offering a paradigm for the development of anti-tumor small-molecule compounds from TCM.

Bufonis Venenum, the dried secretory product from the postauricular and cutaneous glands of Bufonidae, exerts antitumor activity primarily through bufadienolides. This review systematically summarizes the molecular mechanisms of key bufadienolides, including cinobufagin, bufalin, resibufogenin, bufotalin, arenobufagin, gamabufotalin, and cinobufotalin, in the treatment of malignant tumors over the past five years. Current evidence demonstrates that these compounds exert broad-spectrum antitumor effects through multi-target and multi-pathway modulation. In inhibiting tumor cell proliferation, these compounds primarily regulate signaling pathways such as mitogen-activated protein kinase(MAPK), phosphatidylinositol-3-kinase/protein kinase B(PI3K/AKT), and signal transducer and activator of transcription 3(STAT3). In inducing cell death, they eliminate malignant cells through multiple modalities including mitochondrion-mediated apoptosis, ferroptosis, and autophagy. In suppressing invasion and metastasis, they modulate epithelial-mesenchymal transition(EMT), matrix metalloproteinase(MMP) expression, and macrophage polarization within the tumor microenvironment. Furthermore, these compounds inhibit angiogenesis, enhance chemosensitivity, activate antitumor immune responses, and regulate epigenetic modifications. Combination therapy studies reveal that bufadienolides exhibit synergistic efficacy when being combined with clinical chemotherapeutic agents, and TCM preparations containing these compounds demonstrate antitumor properties through multi-target regulation. This review elucidates the antitumor molecular mechanisms of bufadienolides, aiming to provide a theoretical basis for further mechanism investigation and clinical translation.

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.

Cancer treatment urgently requires individualized and precise strategies, and the development of highly selective drugs targeting specific molecular targets has become the core direction of current research. This study focused on the antitumor activity of the flavonoid compound cudratricusxanthone E(CAS 740810-46-2, C7), finding that it can significantly inhibit the proliferation of human cervical cancer HeLa cells in a time-dependent manner. Through the intervention of different cell death inhibitors, this study preliminarily revealed the potential pathway by which C7 induced cell death. The experiments found that the autophagy inhibitor chloroquine effectively blocked C7-mediated cell death, whereas the apoptosis inhibitor z-Val-Ala-Asp(OMe)-fluoromethylketone(Z-VAD-FMK) and the necroptosis inhibitor necrostatin-1(Nec-1) showed no significant effect. This suggested that C7 primarily induced cell death by activating the autophagy pathway, rather than through apoptosis or necroptosis, providing a key clue for understanding the compound's mechanism of action. To further elucidate its molecular mechanism, the study combined network pharmacology predictions with dual-luciferase reporter gene assays, identifying for the first time that the retinoid X receptor α(RXRα) was the target of C7. RXRα is a key regulatory factor in the nuclear receptor family, playing multiple roles in cell proliferation, differentiation, and metabolic regulation. In recent years, it has also been found to have regulatory significance in certain tumor processes. Subsequent experiments confirmed that C7 specifically bound to RXRα, triggering the phosphorylation of downstream adenosine monophosphate-activated protein kinase(AMPK). The activation of AMPK, as a central hub in cellular energy homeostasis and autophagy initiation, significantly promoted autophagic flux. Therefore, C7 drove autophagic cell death in HeLa cells by activating the RXRα/AMPK signaling axis, thereby exerting its antitumor effects. In summary, this study systematically elucidates the novel mechanism by which C7 induces tumor cell death, revealing the complete signaling pathway from the compound targeting RXRα to AMPK activation and ultimately leading to autophagic cell death.

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

Objective: To investigate the efficacy and safety of combination immunotherapy in patients with locally advanced esophageal cancer. Methods: Clinical data of 212 patients with pathologically confirmed locally advanced esophageal cancer who received definitive chemoradiotherapy without surgery at the Affiliated Cancer Hospital of Xinjiang Medical University from January 2019 to January 2024 were retrospectively collected. Follow-up ended in January 2025. Patients were divided into an immunotherapy group (IO group, n=93) and a non-immunotherapy group (Non-IO group, n=119) based on whether immune checkpoint inhibitors were combined during treatment. Propensity score matching (PSM) was used to balance intergroup differences. Cox proportional hazards regression models were applied to identify independent factors influencing progression-free survival (PFS) and overall survival (OS). Results: Before PSM, among the 212 patients, the median PFS was not reached in the IO group, while it was 27.40 months in the Non-IO group. The 1-year PFS rate was significantly better in the IO group than in the Non-IO group (82.4% vs 72.3%; HR=0.65, P=0.048). The median OS was 37.37 months in the IO group and 30.17 months in the Non-IO group, with no statistically significant difference in 1-year OS rates (86.2% vs 82.6%; HR=0.66, P=0.064). After PSM, the median PFS remained unreached in the IO group (n=68), while it was 18.43 months in the Non-IO group (n=68). The IO group maintained its advantage in 1-year PFS rate (80.6% vs 73.7%; HR=0.53, P=0.017). Regarding OS, the median OS was 37.37 months in the IO group and 30.17 months in the Non-IO group, with 1-year OS rates of 84.5% and 90.8%, respectively; the difference was not statistically significant (HR=0.74, P=0.261). Multivariable analysis showed that combination immunotherapy was associated with better PFS (HR=0.49, P=0.010), but no association with OS was observed (HR=0.68, P=0.187). Additionally, N stage and smoking status were independent factors for PFS. Compared with squamous cell carcinoma, patients with non-squamous cell carcinoma had worse OS (HR=4.33, P=0.018). In terms of safety, there were no statistically significant differences between the IO group (n=68) and the Non-IO group (n=68) in the incidence of any-grade adverse events or grade ≥3 adverse events (all P＞0.05). However, the incidence of grade ≥3 lymphocytopenia was significantly higher in the IO group than in the Non-IO group (42.6% vs 19.1%; χ²=8.82, P=0.003). Conclusion: Compared with chemoradiotherapy alone, chemoradiotherapy combined with immunotherapy improves PFS in patients with locally advanced esophageal cancer, but is associated with a higher proportion of patients with severe lymphocytopenia.

Antibody-drug conjugates (ADCs) are covalently conjugated molecules composed of a monoclonal antibody, a payload, and a linker. They represent an innovative therapeutic approach that combines the precise targeting capability of target therapies with the cytotoxic effects of chemotherapeutic agents. Given the unique molecular structure of ADCs, drug-related adverse reactions have drawn a considerable attention. Based on the safety data of ADCs currently available in the field of lung cancer, the common adverse drug reactions primarily involve the digestive system, hematologic system, hepatobiliary system, pulmonary system, skin, eyes, sensory nervous system, and musculoskeletal system. Unlike other cancer types, lung cancer is characterized by complex disease subtypes and molecular pathological mechanisms, as well as diverse treatment modalities. Moreover, patients with advanced lung cancer often have comorbidities such as chronic obstructive pulmonary disease and pulmonary inflammation, making the comprehensive management of ADC-related adverse reactions even more challenging. To address this, the Precision Treatment Branch of Thoracic Oncology, Chinese Geriatric Health Association, has taken the lead in organizing a multidisciplinary panel of domestic experts in gastroenterology, dermatology, respiratory medicine, ophthalmology and oncology, to discuss and jointly formulate the "Consensus of Chinese experts on the multidisciplinary management of adverse reactions to antibody-drug conjugates in the treatment of Lung Cancer (2025 edition)". A total of 21 recommendations are proposed in this consensus, covering pre-ADC safety assessments, comprehensive monitoring and management of relevant adverse reactions during ADC treatment, patient education, and medication guidance for special populations. The consensus aims is to provide clinicians with practical guidelines for the application of ADC, thereby maximizing therapeutic benefits for patients with lung cancer.

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.

The rearranged during transfection (RET) gene is a proto-oncogene encoding a receptor tyrosine kinase. RET gene alterations are driver events in various tumors. Pralsetinib and selpercatinib are novel, highly selective RET tyrosine kinase inhibitors (RET-TKIs). They are recommended as priority therapeutic options for RET fusion-positive non-small cell lung cancer (NSCLC) in the Chinese Society of Clinical Oncology (CSCO) Guidelines for the Diagnosis and Treatment of Non-Small Cell Lung Cancer and Thyroid Carcinoma and the Chinese Medical Association (CMA) Clinical Guidelines for Lung Cancer, as well as for radioiodine-refractory differentiated thyroid cancer with RET fusion and RET-mutant medullary thyroid carcinoma. Common adverse events asosociated with pralsetinib and selpercatinib include hypertension, liver enzyme abnormalities, neutropenia and fatigue. Studies have demonstrated that the incidence of adverse events is not associated with disease type. Given the low prevalence of RET gene alterations (＜5%), which are regarded as rare genetic mutations, clinical experience in the use pf RET-TKIs and and patient management remains limited. Base on the current status of adverse event management of RET-TKIs in China, and integrating the latest international evidence and clinical experience, the Chinese Medical Doctor Association Tumor Multidisciplinary Diagnosis and Treatment Professional Committee and the Shenzhen Medical Doctor Association Tumor Multidisciplinary Diagnosis and Treatment Professional Committee organized discussion among experts from medical oncology, respiratory medicine, radiation oncology, thoracic surgery, and other related disciplines to formulate this expert consensus on the management of adverse events of RET-TKIs.

To investigate the effect and potential mechanism of blueberry anthocyanins(BA) in enhancing the chemosensitivity of colon cancer cells to oxaliplatin(OXA).

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.

Immune checkpoint inhibitors(ICIs) have become a significant breakthrough in cancer therapy by activating anti-tumor immune responses through the blockade of immune checkpoint molecules. However, acquired resistance to ICIs and immune-related adverse events(irAEs) severely limit their clinical application. TCM, based on the principles of holistic view and syndrome differentiation-based treatment, demonstrates distinct advantages in enhancing ICIs efficacy due to its unique immunomodulatory effects and multi-target, multi-pathway mechanisms. Studies suggest that TCM may effectively enhance T cell-mediated anti-tumor activity and improve ICIs resistance through various mechanisms, including modulating the tumor microenvironment, intervening in key immune signaling pathways, and restoring gut microbiota homeostasis. Additionally, TCM shows promising potential in alleviating ICIs-induced irAEs, such as colitis, pneumonitis, and cardiotoxicity, thereby improving patient tolerance to treatment. This review systematically summarizes the synergistic mechanisms and recent research progress in the combined use of TCM and ICIs, aiming to provide novel insights for optimizing cancer immunotherapy strategies. In the future, a precision medicine model integrating TCM and western medicine may offer safer and more effective therapeutic options for cancer patients, further advancing the development of tumor immunotherapy.

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.