Jiehua Li

GALNT1, a key enzyme mediating O-GalNAc glycosylation, has not been fully characterized in the tumor microenvironment. This study aimed to investigate its expression pattern, molecular mechanisms, and clinical relevance in breast cancer. Public datasets (TCGA, GEO, CPTAC) and single-cell transcriptomic data were integrated to analyze GALNT1 expression across cancer types and at the single-cell resolution. The expression and subcellular localization of GALNT1 in breast cancer were verified using qRT-PCR, Western blot, and immunofluorescence staining. Functional assays were conducted to assess its effects on cell proliferation, migration, and O-glycosylation, while CCK-8 assays were used to evaluate sensitivity to bortezomib. GALNT1 was significantly upregulated in primary breast cancer as well as multiple other malignancies. In vitro experiments demonstrated that GALNT1 promoted breast cancer cell proliferation, migration, and O-glycosylation. Immunofluorescence staining revealed widespread GALNT1 expression in tumor epithelial cells and cancer-associated fibroblasts (CAFs), with colocalization to the Tn antigen. Notably, GALNT1-mediated O-glycosylation was associated with resistance to bortezomib. High GALNT1 expression correlated with increased infiltration of CAFs and M2 macrophages, and reduced CD8⁺ T cell infiltration. Single-cell transcriptomic analysis further confirmed CAF-specific enrichment and elevated epithelial-mesenchymal transition (EMT) scores. GALNT1 is highly expressed in breast cancer, where it promotes tumor progression, bortezomib resistance through O-glycosylation, and immune microenvironment remodeling. The data imply that GALNT1 could represent a novel therapeutic candidate in breast cancer. The online version contains supplementary material available at 10.1007/s00432-026-06448-2.

Objective: Medullary thyroid carcinoma is a rare malignancy with heterogenous outcomes, and the existing American Joint Committee on Cancer staging system does not adequately incorporate patient- or treatment-specific prognostic factors. Methods: Patients with medullary thyroid carcinoma were identified from the Surveillance, Epidemiology, and End Results database and randomly assigned to derivation and validation groups. Five prognostic approaches, including Cox regression, least absolute shrinkage and selection operator-Cox, CoxBoost, random survival forest, and extreme gradient boosting, were evaluated using Harrell’s concordance index. Least absolute shrinkage and selection operator-Cox, which demonstrates optimal performance and simplicity, was selected to develop a nomogram to predict 3- and 5-year mortality. Results: A total of 4157 patients were included, with 2938 assigned to the derivation group and 1219 to the validation group. The least absolute shrinkage and selection operator-Cox model demonstrated strong predictive performance, yielding Harrell’s concordance indices of 0.813 and 0.852, both exceeding those of American Joint Committee on Cancer staging (0.730 and 0.722). Calibration plots showed close agreement between predicted and observed mortality, and decision curve analysis revealed that the nomogram provided a higher net benefit compared with strategies of treating all or no patients. Conclusion: A nomogram integrating demographic, clinical, and treatment factors was developed to predict individual survival in medullary thyroid carcinoma, providing complementary information to American Joint Committee on Cancer staging and facilitating personalized risk stratification.

Background: Metastasis to lymph nodes posterior to the right recurrent laryngeal nerve (LN-prRLN) in papillary thyroid carcinoma (PTC) presents significant surgical challenges due to its deep anatomical location and association with disease recurrence. Objective: To identify risk factors for LN-prRLN metastasis and develop a validated prediction model for clinical decision-making. Methods: A retrospective analysis of 341 PTC patients underwent LN-prRLN dissection (May 2022–September 2024) at the First Affiliated Hospital of Guangxi Medical University was conducted. Clinicopathological characteristics were compared between metastasis-positive and negative groups. Independent risk factors were identified through univariate and multivariate logistic regression and utilized to construct a nomogram. Model performance was assessed using Receiver operating characteristic (ROC) curves, calibration plots, and decision curve analysis (DCA). Results: Male (odds ratio = 2.670, 95%CI:1.094–6.516), Tumor diameter (odds ratio = 1.931, 95%CI:1.140–3.270), Multifocality (odds ratio = 3.658, 95%CI:1.251–10.692), LN-arRLN metastasis (odds ratio = 1.340, 95%CI:1.122–1.602), Lateral lymph node metastasis (odds ratio = 7.815, 95%CI:2.857–21.379), Extrathyroidal extension (OR = 3.627, 95%CI:1.133–11.611) were identified as the independent risk factors for LN-prRLN metastasis. The nomogram demonstrated excellent discrimination (AUC: training cohort = 0.889; validation cohort = 0.858). The calibration curves demonstrated good concordance between predicted probabilities and the actual observed probabilities. The DCA curve indicates robust clinical utility for the model. Conclusion: This study extends prior research by identifying additional independent risk factors, the model evaluation results indicated satisfactory predictive performance, facilitates individualized surgical planning to balance therapeutic efficacy against procedural risks.

Preeclampsia has been associated with a reduced risk of breast cancer (BC), but the mechanisms underlying this relationship remain unclear. It has been suggested that neutrophil extracellular traps (NETs), which are released upon neutrophil activation, play a key role in both preeclampsia and BC. To investigate this link, the single‑cell RNA sequencing dataset GSE173193 was analyzed and upregulated genes BCL2A1 and G0/G1 switch gene 2 (G0S2) were identified in neutrophils from preeclamptic placentas. These findings were validated using reverse transcription‑quantitative PCR and western blotting. Combined analyses of preeclampsia and BC tissues, from Gene Expression Omnibus (GSE24129) and The Cancer Genome Atlas databases respectively, identified 2,040 upregulated differentially expressed genes, including BCL2A1 and G0S2. Furthermore, these genes showed clinical relevance to BC, as demonstrated by Receiver Operating Characteristic curve, survival analyses and weighted gene co‑expression network analysis. Functional experiments revealed that overexpression of BCL2A1 and G0S2 increased NET release and inhibited BC cell proliferation, invasion and migration. The present study provides novel insights into the shared molecular pathways of preeclampsia and BC, emphasizing NETs as a potential protective mechanism as increased NET production in preeclampsia may contribute to a reduced BC risk by influencing tumor progression and offer avenues for further research into therapeutic interventions.

Background: Gastric cancer (GC) remains a major global health concern, with limited treatment options, especially in advanced stages. Radiotherapy (RT) plays a vital role in GC management, but resistance to DNA damage impedes its effectiveness. MicroRNA-1284 (miR-1284), a tumor suppressor, regulates eukaryotic translation initiation factor 4A1 (EIF4A1), which is involved in DNA damage repair through homologous recombination (HR). This axis has been implicated in enhancing GC cell survival following RT. Additionally, the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway, activated by DNA damage, plays a key role in triggering an anti-tumor immune response. However, the interaction between the miR-1284/EIF4A1 axis, DNA repair, and the cGAS-STING pathway in GC under RT conditions remains unclear. This study aims to investigate how the miR-1284/EIF4A1 axis influences DNA repair and its role in activating the cGAS-STING pathway to enhance RT efficacy in GC. Methods: A stably expressed messenger miR-1284 cell line was established. Quantitative reverse transcription and western blot were used to examine the expression of miR-1284 and EIF4A1, and the effect of blocking the miR-1284/EIF4A1 axis on the cGAS-STING pathway and interferon-β (IFN-β) in GC cells after RT; cytotoxicity experiments were conducted to explore the mechanism of the miR-1284/EIF4A1 axis in radiation-induced DNA damage repair; animal experiments were conducted to explore the translational application of rocaglamide (RocA) combined with the programmed cell death-ligand 1 (PD-L1) antibody in RT. Results: The miR-1284/EIF4A1 axis in the GC cells promoted the repair of radiation-induced DNA damage and was associated with the prognosis of GC patients. Blocking this axis delayed the C-terminal binding protein interacting protein (CtIP)-mediated DNA repair, enhanced RT effectiveness, and activated the cGAS-STING pathway, while increasing the rate of apoptosis. In vivo experiments based on RocA binding to PD-L1 antibodies under RT had good biological safety, and thus provide a potential therapeutic strategy for the treatment of GC. Conclusions: The miR-1284/EIF4A1 axis promotes the repair of DNA damage caused by RT, promotes the activation of the cGAS-STING pathway in GC, and has good biological safety. Our findings provide an important experimental basis for enhancing the anti-tumor immune effect of RT in the treatment of GC.

Breast cancer has emerged as the primary cause of mortality stemming from malignancies among women. HuaChanSu has demonstrated efficacy in suppressing the progression of various malignancies. However, the specific immune targets and pathways influenced by HuaChanSu within mammary tumors remain elusive. This study is designed to uncover potent monomers and pivotal targets associated with HuaChanSu’s anti-breast cancer Immunotherapy. The genes pertinent to HuaChanSu and breast cancer were acquired individually from publicly available databases. Interaction analysis using Cytoscape was conducted on common genes to determine the most suitable targets and crucial constituents of HuaChanSu’s Immunotherapy against breast cancer. Following this, molecular docking was employed to validate ligand and receptor binding interactions. Lastly, the identified core genes underwent assessment of immune infiltration. The intersection of HuaChanSu and BC targets yielded a total of 49 differentially expressed genes. Bufalin emerged as the most potent constituent in Immunotherapy. Immunoassay data demonstrated significant correlations (r > 0.03, p < 0.05) between S100B, MMP9, FOS, EGFR, KIT, MME, and immune infiltration within BC. Molecular docking further corroborated the effective binding of Bufalin with immune-related genes. Through network pharmacological validation, we propose the extraction of Bufalin, a monomeric constituent of Huachansu, to exert immunomodulatory effects aimed at inhibiting the progression of breast cancer. Most of the target genes (S100B, BIRC5, MMP9, FOS, EGFR, KIT, and MME) are common targets for immunotherapy.

Objective: To investigate contralateral central lymph node metastasis (CCLNM) in patients with unilateral papillary thyroid carcinoma (UPTC). To provide a reference for clinical decision-making, a prediction model for the probability of CCLNM was established. Method: The clinicopathological data of 221 UPTC patients who underwent surgical treatment were retrospectively analyzed. Univariate and multivariate logistic regression analyses were performed to determine the independent risk factors for CCLNM according to clinicopathological characteristics, construct a prediction model to construct a visual nomogram, and evaluate the model. Results: According to univariate and multivariate logistic regression analyses, sex (P = 0.01, OR: 3.790, 95% CI: 1.373–10.465), extrathyroidal tumor extension (ETE) (P = 0.040, OR: 6.364, 95% CI: 1.083–37.381), tumor diameter (P = 0.010, OR: 3.674, 95% CI: 1.372–9.839) and ipsilateral central lymph node metastasis (ICLNM) (P < 0.001, OR: 38.552, 95% CI: 2.675–27.342) were found to be independent risk factors for CCLNM and were used to construct a nomogram for internal verification. The ROC curve had an AUC of 0.852 in the training group and an AUC of 0.848 in the verification group, and the calibration curve indicated that the prediction probability of the model was consistent with the actual probability. Finally, the analysis of the decision curve showed that the model has good application value in clinical decision-making. Conclusion: Sex, ETE, tumor size, and ICLNM emerged as independent risk factors for CCLNM in UPTC patients. A predictive model was therefore developed, harnessing these variables to enable an objective, personalized estimation of CCLNM risk. This tool offers valuable insights to inform surgical planning and optimize treatment strategies for UPTC management.

Objective To understand the current status of occupational stress, occupational burn-out and sleep quality among ambulance drivers in Hengyang, China and to analyse the relationship between occupational stress, occupational burn-out and sleep quality of ambulance drivers. Design A cross-sectional study. Setting Prehospital emergency centre of third-class hospital in Hengyang, China. Participants From October 2023 to December 2023, a cross-sectional survey was conducted, with 213 ambulance drivers from Hengyang, China, selected as participants. Methods General demographic questionnaires, the Chinese Occupational Stress Inventory, the Maslach Burnout Inventory and the Pittsburgh Sleep Quality Index were used for data collection and analysis. Results Occupational stress among ambulance drivers was positively correlated with occupational burn-out and sleep quality (r=0.528, 0.447, both pConclusion The sleep quality of ambulance drivers in Hengyang, China is suboptimal, with occupational stress directly predicting sleep quality. Occupational burn-out plays a partial positive mediating role between occupational stress and sleep quality among ambulance drivers. Reducing occupational stress and burn-out is beneficial for improving the sleep quality of ambulance drivers.