Liangdan Tang

Construction and Validation of a Nomogram to Predict the Postoperative Venous Thromboembolism Risk in Patients with HGSOC

Venous thromboembolism (VTE) is a common complication in patients with high-grade serous ovarian cancer (HGSOC) after surgery. This study aims to establish a comprehensive risk assessment model to better identify the potential risk of postoperative VTE in HGSOC. Clinical data from 587 HGSOC patients who underwent surgical treatment were retrospectively collected. Univariate and multivariate logistic regression analyses were performed to identify independent factors influencing the occurrence of postoperative VTE in HGSOC. A nomogram model was constructed in the training set and further validated in the verification set. Logistic regression identified age (odds ratio [OR] = 1.063, P  = .002), tumor size (OR = 3.815, P  < .001), postoperative transfusion (OR = 5.646, P  = .001), and postoperative D-dimer (OR = 1.246, P  = .003) as independent risk factors for postoperative VTE in HGSOC patients. A nomogram was constructed using these factors. The receiver operating characteristic curve showed an area under the curve (AUC) of 0.840 (95% confidence interval [CI]: 0.782, 0.898) in the training set and 0.793 (95% CI: 0.704, 0.882) in the validation set. The calibration curve demonstrated a good consistency between model predictions and actual results. The decision curve analysis indicated the model benefits at a threshold probability of less than 70%. A nomogram predicting postoperative VTE in HGSOC was established and validated. This model will assist clinicians in the early identification of high-risk patients, enabling the implementation of appropriate preventive measures.

Molecular mechanisms by which C1orf112 promotes endometrial cancer progression and the development and validation of a clinical scoring model

To investigate the expression profile, clinical significance, and underlying molecular mechanisms of C1orf112 in endometrial cancer (EC). We performed bioinformatics analyses using data from The Cancer Genome Atlas to evaluate C1orf112 expression and its association with clinicopathological parameters in EC. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses, as well as protein-protein interaction network analysis, were conducted to explore the functional roles and regulatory pathways of C1orf112. A multi-omics integrative approach was used to elucidate the regulatory mechanisms underlying C1orf112 expression. Furthermore, we constructed and validated a prognostic scoring model incorporating C1orf112 expression. C1orf112 was found to be significantly highexpressed in EC tissues and its expression was closely associated with clinical stage, histological grade, and patient prognosis. Functional enrichment analyses indicated that C1orf112 and its co-expressed genes are primarily involved in cell cycle regulation, DNA replication, and the p53 signaling pathway. Notably, our bioinformatics predictions suggest that C1orf112 may be subject to bidirectional regulation by RNA-binding proteins, including LIN28B and SRRM4, potentially establishing a regulatory balance between oncogenic and tumor-suppressive pathways. Multi-omics analysis demonstrated that C1orf112 expression is co-regulated by genetic alterations and epigenetic modifications, with promoter DNA methylation levels showing a strong inverse correlation with transcriptional activity. However, further molecular and phenotypic validation is required to confirm these interactions. The prognostic scoring model incorporating C1orf112 expression exhibited robust predictive performance. Our findings highlight the potential clinical utility of C1orf112 as a diagnostic and prognostic biomarker in EC, and provide new insights into its regulatory molecular network. This study proposes a conceptual framework for understanding EC pathogenesis and guiding the development of targeted therapies. Nonetheless, further prospective clinical studies and mechanistic investigations are warranted to validate these findings.

Nck1 promotes the progression of ovarian carcinoma by enhancing the PI3K/AKT/p70S6K signaling

Non-catalytic region of tyrosine kinase adaptor protein 1 (Nck1) is crucial for the progression of cancers. However, little is known on the role of Nck1 in the progression of ovarian carcinoma (OC). Here, we show that Nck1 expression is up-regulated in 176 OC tissues, compared with non-carcinoma ovarian tissues, and the up-regulated Nck1 expression is associated with the aggressiveness of OC and shorter overall and disease-free survival in this population. Higher Nck1 expression was an independent risk factor for poor prognosis of OC. Furthermore, Nck1 silencing by short hairpin RNA (shRNA) technology significantly inhibited the proliferation, migration and invasion of OC cells in vitro and the growth and metastasis of implanted OC tumors in vivo. Human kinase phosphorylation array indicated that Nck1 silencing significantly reduced the relative levels of 11 kinase expression and phosphorylation in OC cells, particularly for decreased levels of p70S6 kinase (p70S6K) and protein kinase B (AKT) expression in SKOV3 cells. Actually, Nck1 silencing significantly decreased PI3K and AKT expression, and reduced AKT and p70S6K phosphorylation while Nck1 over-expression had opposite effects in OC cells. Therefore, our data indicate that Nck1 promotes the progression of OC by enhancing the PI3k/AKT/p70S6K signaling in OC. Our findings suggest that Nck1 expression may be valuable for evaluating the prognosis of OC and as a target for design of new therapies for OC.