Osteosarcoma (OS) is a primary malignant bone tumor most commonly affecting children and adolescents and is characterized by loss of differentiation. Bone morphogenetic protein/retinoic acid inducible neural-specific 3 (BRINP3) has been reported to regulate the differentiation of osteoblasts. However, the role that BRINP3 plays in the progression of osteosarcoma remains unknown. We found in this study that BRINP3 was highly expressed in 64.13% of human osteosarcoma tissues and it was associated with histological grade, tumor recurrence, and poor clinical prognosis of osteosarcoma. In vitro, downregulation of BRINP3 was able to inhibit the proliferation and invasion of osteosarcoma cell lines. Furthermore, BRINP3 interacted with microtubule-associated protein 4 (MAP4) at the protein level, and overexpression of MAP4 could partially reverse the inhibitory effect of downregulated BRINP3 on the proliferation and invasion of osteosarcoma cells, which indicates that downregulation of BRINP3 might suppress the proliferation and invasion of osteosarcoma cells by inhibiting MAP4 expression. Overall, our results demonstrate that BRINP3 functions as an oncogene within osteosarcoma through MAP4 and could therefore be used as a potential biomarker for osteosarcoma diagnostics and therapeutics.

E15096 Background: Golgi protein 73 (GP73), a membrane protein localized in the type II Golgi complex, is a candidate biomarker for hepatocellular carcinoma (HCC). However, current evidence is conflicting in its diagnostic value as a serum marker for HCC, largely due to the small sample sizes of previous studies. Furthermore, the association between serum GP73 level and prognostic parameters remains unclear. Methods: Serum GP73 levels were measured in 405 patients with HCC, 203 patients with liver cirrhosis, and 98 healthy controls using enzyme-linked immunosorbent assay (ELISA). Its correlation with clinical characteristics was analyzed further. Results: The median serum GP73 levels were 19.59 ng/mL (range, 0–231.17 ng/mL) in patients with HCC, 19.28 ng/mL (range, 0–187.78 ng/mL) in patients with liver cirrhosis, and 0 ng/mL (range, 0–70.42 ng/mL) in healthy controls, respectively. The serum GP73 levels in both HCC and liver cirrhosis groups were higher than those in healthy controls (P < 0.001), whereas...

Biliary tract cancer (BTC) is typically diagnosed at an advanced stage due to the lack of effective screening tools, resulting in limited therapeutic options and poor survival outcomes. Therefore, there is a critical need for non-invasive strategies that enable early detection and risk stratification. Fragmentomic profiling of cell-free DNA (cfDNA) captures genome-wide fragmentation patterns reflecting tumor-associated chromatin structure and genomic instability, providing a promising approach for non-invasive cancer detection. In this study, we developed a low-pass whole-genome sequencing (WGS)-based framework for BTC detection and postoperative risk assessment. Plasma samples were analyzed to derive three fragmentomic features, including copy number variation, fragment size distribution, and promoter fragmentation entropy, which were integrated into a machine-learning model trained using five-fold cross-validation. The model demonstrated robust performance across independent validation cohorts, outperforming individual fragmentomic features and conventional serum biomarkers, and accurately distinguished BTC from benign biliary diseases. Longitudinal analyses revealed that cfDNA fragmentomic risk scores dynamically tracked disease burden and treatment response. Importantly, postoperative risk scores were independently associated with disease-free survival, highlighting their prognostic value. Collectively, these findings establish a scalable and cost-effective framework for cfDNA-based BTC detection and monitoring using low-pass WGS data. This approach shows strong potential for targeted screening in high-risk populations and for guiding personalized postoperative surveillance and clinical management for BTC patients.