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Towards Evaluation Engineering: An Empirical Study of ML Evaluation Harnesses in the Wild
CollectionLoRA: Collecting 50 Effects in 1 LoRA via Multi-Teacher On-Policy Distillation
Efficient and Scalable Neural Symbolic Search for Knowledge Graph Complex Query Answering
Kolmogorov-Arnold Fourier Networks
PiXTime: A Model for Federated Time Series Forecasting with Heterogeneous Data across Nodes
BEAR: Towards Beam-Search-Aware Optimization for Recommendation with Large Language Models
Prism: Spectral-Aware Block-Sparse Attention
PRXL2B facilitates the progression of hepatocellular carcinoma and the therapeutic efficacy of oncolytic adenovirus H101 through the PI3K/AKT/PD-L1 axis
Biosci Trends. 2026 May 21. doi: 10.5582/bst.2026.01000. Online ahead of print.
ABSTRACT
Oncolytic adenovirus H101 has shown antitumor activity in hepatocellular carcinoma (HCC), but the molecular determinants of treatment response remain unclear. In this study, a Hepa1-6 subcutaneous tumor model was established in C57BL/6 mice and treated with intratumoral H101, followed by integrated transcriptomic and proteomic analyses to identify candidate genes associated with H101 response. PRXL2B was selected for further investigation using public multi-omics datasets, tissue microarray-based immunohistochemistry, in vitro functional assays, mechanistic analyses, and in vivo validation experiments. Integrated multi-omics analyses identified PRXL2B as a candidate gene downregulated after H101 treatment. Public datasets and tissue-based validation further showed that PRXL2B was upregulated in HCC tissues. In MHCC97H and HCCLM3 cells, PRXL2B knockdown inhibited proliferation, migration, and invasion, promoted apoptosis and cell-cycle arrest, and enhanced the antitumor effect of H101. Mechanistically, PRXL2B silencing reduced AKT phosphorylation and PD-L1 expression. In vivo, PRXL2B knockdown suppressed tumor growth, and the combination of PRXL2B knockdown and H101 produced the strongest antitumor effect. These findings indicate that PRXL2B promotes malignant phenotypes in HCC and may modulate H101 efficacy through the PI3K/AKT/PD-L1 axis. Targeting PRXL2B may therefore represent a potential strategy to enhance the therapeutic efficacy of oncolytic virus therapy in HCC.
PMID:42161529 | DOI:10.5582/bst.2026.01000
Proteomic and lipidomic analyses reveal molecular subtypes and potential targets in early-stage lung adenocarcinoma among non-smokers
Cell Rep. 2026 May 26;45(5):117215. doi: 10.1016/j.celrep.2026.117215. Epub 2026 Apr 28.
ABSTRACT
Early-stage lung adenocarcinoma (LUAD) in never smokers exhibits distinct biological features, yet the metabolic programs driving early invasion remain unclear. We integrate proteomic and lipidomic profiling of primary LUAD tumors from never smokers, matched normal adjacent tissues (NATs), and benign pulmonary nodules (BPNs). Integrated multi-omics analysis reveals coordinated dysregulation of lipid metabolism and immune signaling in early LUAD. Proteome-based network fusion stratifies invasive LUAD into immune-metabolic synergistic (IMS) and metabolic-stress-driven (MSD) subtypes. IMS tumors retain apolipoprotein-associated lipid modules and favorable immune features, whereas MSD tumors exhibit stress-response programs. Mechanistically, APOA1 and APOC1 emerge as key nodes linking lipid homeostasis to invasion, and their depletion promotes LUAD cell migration and invasion. We establish a two-protein, four-lipid diagnostic panel demonstrating robust performance across tissue and plasma cohorts. These findings provide a molecular basis for early detection and risk stratification in never smokers.
PMID:42054209 | DOI:10.1016/j.celrep.2026.117215
SREBP2 regulates CCDC25 expression and promotes tumor metastasis in Triple-Negative Breast Cancer
Oncogenesis, Published online: 13 April 2026; doi:10.1038/s41389-026-00614-4
SREBP2 regulates CCDC25 expression and promotes tumor metastasis in Triple-Negative Breast CancerAn activated wheat CCG10-NLR immune receptor forms an octameric resistosome
Safe Decentralized Operation of EV Virtual Power Plant with Limited Network Visibility via Multi-Agent Reinforcement Learning
SecPI: Secure Code Generation with Reasoning Models via Security Reasoning Internalization
Restoring circadian rhythms in the hypothalamic paraventricular nucleus reverses aging biomarkers and extends lifespan in male mice
Genetically encoded fluorescent reporters to visualize α-synuclein pathology in live brain
Interview-Informed Generative Agents for Product Discovery: A Validation Study
Generative Data Transformation: From Mixed to Unified Data
STAT3-mediated transactivation of NOVA2 promotes lung adenocarcinoma metastasis by splicing SMAD4
Oncogene, Published online: 01 April 2026; doi:10.1038/s41388-026-03752-6
STAT3-mediated transactivation of NOVA2 promotes lung adenocarcinoma metastasis by splicing SMAD4