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From Cross-Task Examples to In-Task Prompts: A Graph-Based Pseudo-Labeling Framework for In-context Learning
Generative AI for Healthcare: Fundamentals, Challenges, and Perspectives
Genotype-Phenotype Integration through Machine Learning and Personalized Gene Regulatory Networks for Cancer Metastasis Prediction
Integrating Genomics into Multimodal EHR Foundation Models
Quanvolutional Neural Networks for Pneumonia Detection: An Efficient Quantum-Assisted Feature Extraction Paradigm
Closing Gaps: An Imputation Analysis of ICU Vital Signs
Dynamic Monitoring of Recurrent Ovarian Cancer Using Serial ctDNA: A Real-World Case Series
Curr Oncol. 2025 Oct 21;32(10):585. doi: 10.3390/curroncol32100585.
ABSTRACT
Recurrent ovarian cancer (OC) is challenging to detect early using current methods like CA-125 and imaging. Circulating tumor DNA (ctDNA) may improve disease monitoring. Here, we assess the real-world clinical utility of serial ctDNA analyses in patients with recurrent OC. We analyzed serial plasma samples (N = 23) from six patients with recurrent OC using a tumor-informed next-generation sequencing assay targeting 68 cancer-related genes developed at the University of Washington. ctDNA variant allele frequencies (VAFs) were correlated with CA-125 levels, radiographic findings, and clinical outcomes. ctDNA levels generally reflected clinical status, accurately mirroring disease progression and therapeutic response. In one patient, rising ctDNA preceded clinical recurrence by four months, despite normal CA-125 and imaging, highlighting its potential advantage. Conversely, some patients exhibited clinical progression with undetectable ctDNA, indicating limitations in assay sensitivity, biological factors, or metastatic sites (e.g., brain metastases). ctDNA and CA-125 showed complementary value in most cases, suggesting potential combined use in clinical monitoring. Our findings demonstrate that ctDNA is a promising biomarker to complement existing monitoring approaches for recurrent OC. In some cases, capable of predicting relapse and treatment response ahead of current clinical indicators. However, identified discordances underscore technical and biological challenges that warrant further investigation. Larger prospective studies are necessary to refine ctDNA's clinical utility and integration into personalized OC care.
PMID:41149505 | PMC:PMC12563156 | DOI:10.3390/curroncol32100585
Tongyi DeepResearch Technical Report
Agent Data Protocol: Unifying Datasets for Diverse, Effective Fine-tuning of LLM Agents
The Confidence Paradox: Can LLM Know When It's Wrong
The Role of Omentin in Gastrointestinal Cancer: Diagnostic, Prognostic, and Therapeutic Perspectives
Metabolites. 2025 Sep 30;15(10):649. doi: 10.3390/metabo15100649.
ABSTRACT
Background/Objectives: Omentin, also known as intelectin-1, is a secreted adipokine with anti-inflammatory, insulin-sensitizing, and immune-modulatory functions, primarily expressed in visceral adipose tissue. While omentin has been associated with favorable metabolic outcomes, its role in cancer pathogenesis appears context-dependent and remains poorly understood. This review investigates the biological functions, expression patterns, and clinical relevance of omentin across gastrointestinal malignancies. Methods: A comprehensive review of the literature was conducted using PubMed, Scopus, and Web of Science up to August 2025 to evaluate the role of omentin in gastrointestinal cancers. Both preclinical and clinical studies evaluating omentin, its analogues and omentin-enhancing agents in gastric, colorectal, hepatic, pancreatic, and esophageal cancers were included. Results: Omentin exhibits anti-proliferative, anti-inflammatory, and anti-angiogenic effects within the tumor microenvironment in several GI malignancies. However, evidence also indicates a dual role. High intratumoral omentin expression correlates with improved prognosis in colorectal, gastric, and hepatic cancers; in contrast, elevated circulating levels-particularly in colorectal and pancreatic cancers-have been paradoxically associated with increased cancer risk and poor outcomes. Mechanistically, omentin modulates PI3K/Akt, NF-κB, AMPK, and oxidative stress pathways, and interacts with TMEM207. However, most available studies are small-scale and heterogeneous, with methodological inconsistencies and limited multi-omics integration, leaving major knowledge gaps. Conclusions: This review highlights omentin's distinct systemic and local roles across GI cancers, underscoring its translational implications. Omentin emerges as a promising but context-dependent biomarker and therapeutic target, with future research needed to address heterogeneity, standardize assays, and validate its clinical utility in large-scale prospective studies.
PMID:41149627 | PMC:PMC12566161 | DOI:10.3390/metabo15100649