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SSDAU: Structured Semantic Data Augmentation for Joint Entity and Relation Extraction
Clinical and translational roles of circulating tumor cells in non-small cell and small cell lung cancer: a narrative review
J Thorac Dis. 2026 Apr 30;18(4):415. doi: 10.21037/jtd-2026-1-0025. Epub 2026 Apr 24.
ABSTRACT
BACKGROUND AND OBJECTIVE: Circulating tumor cells (CTCs) are malignant cells shed into blood that enable noninvasive, longitudinal assessment of lung cancer. Increasing evidence frames CTCs within a circulating tumor microenvironment (cTME) and broader circulating tumor-associated cell (CTAC) ecosystems that include multicellular clusters and circulating tumor endothelial cells (CTECs). We summarize definitions, detection approaches, and clinical applications of CTC-centered liquid biopsy in non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC).
METHODS: A comprehensive literature search was conducted in PubMed, Embase, Web of Science, and Google Scholar using the terms "non-small cell lung cancer", "small cell lung cancer", and "circulating tumor cells". Relevant clinical, basic, and translational studies were selected and synthesized to outline current knowledge and future directions.
KEY CONTENT AND FINDINGS: CTCs can be enriched by immunoaffinity, size, or microfluidic platforms, enabling enumeration and downstream profiling. In both NSCLC and SCLC, CTC positivity and higher burden are associated with worse survival, with the strongest effects in SCLC and with circulating tumor emboli (CTE). Serial monitoring provides early signals of response or failure; and post-treatment supports minimal residual disease (MRD) detection and relapse prediction. Molecular and phenotypic profiling enables driver and resistance tracking, including epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), while CTECs may add vascular and immune-relevant information.
CONCLUSIONS: CTC-based assays have the potential to complement imaging and tissue biopsy across screening research, prognostication, therapeutic monitoring, MRD assessment, and personalized care. Clinical translation requires standardized preanalytical workflows, harmonized thresholds, and prospective trials testing CTC-guided management.
PMID:42182710 | PMC:PMC13190041 | DOI:10.21037/jtd-2026-1-0025
Machine learning-driven multi-omics integration uncovers a senescence associated molecular axis in HCC
Front Immunol. 2026 May 8;17:1762222. doi: 10.3389/fimmu.2026.1762222. eCollection 2026.
ABSTRACT
BACKGROUND: Hepatocellular carcinoma (HCC) exhibits profound molecular heterogeneity and aberrant cellular senescence. This study systematically dissects the senescence-associated molecular landscape to identify key regulators driving HCC progression and immune evasion.
METHODS: Integrating multi-cohort transcriptomic datasets, we developed a robust prognostic signature using 101 machine-learning models, identifying prognostic signature. We employed preliminary proteomic, exploratory metabolomic, and single-cell RNA sequencing (scRNA-seq) analyses to explore multi-omics alterations. The functional senescence status and MCM7 were validated in a clinical HCC cohort by RT-qPCR, Western blotting, immunohistochemistry, and multiplex immunofluorescence (mIF). Causality was established using in vitro functional assays in HepG2 cells.
RESULTS: A 12-gene random survival forest (RSF) signature accurately predicted patient survival across independent cohorts. MCM7 emerged as a central senescence-associated driver. ScRNA-seq and mIF confirmed MCM7 characterizes a highly proliferative, clonally expanding subset of CD8+ T cells within the tumor microenvironment. In vitro, MCM7 knockdown significantly inhibited HepG2 cell proliferation and upregulated senescence enforcers p16 and p21, whereas overexpression facilitated evasion. Additionally, TIDE analysis revealed that high-risk patients exhibited elevated immune evasion potential, predicting poor immunotherapy response.
CONCLUSION: This integrative multi-omics framework uncovers an MCM7 MCM7-driven senescence-associated axis promising HCC progression and immune dysfunction, offering a robust tool for prognostic stratification and novel therapeutic insights.
PMID:42183188 | PMC:PMC13195000 | DOI:10.3389/fimmu.2026.1762222
Machine learning-driven multi-omics integration uncovers a senescence associated molecular axis in HCC
Front Immunol. 2026 May 8;17:1762222. doi: 10.3389/fimmu.2026.1762222. eCollection 2026.
ABSTRACT
BACKGROUND: Hepatocellular carcinoma (HCC) exhibits profound molecular heterogeneity and aberrant cellular senescence. This study systematically dissects the senescence-associated molecular landscape to identify key regulators driving HCC progression and immune evasion.
METHODS: Integrating multi-cohort transcriptomic datasets, we developed a robust prognostic signature using 101 machine-learning models, identifying prognostic signature. We employed preliminary proteomic, exploratory metabolomic, and single-cell RNA sequencing (scRNA-seq) analyses to explore multi-omics alterations. The functional senescence status and MCM7 were validated in a clinical HCC cohort by RT-qPCR, Western blotting, immunohistochemistry, and multiplex immunofluorescence (mIF). Causality was established using in vitro functional assays in HepG2 cells.
RESULTS: A 12-gene random survival forest (RSF) signature accurately predicted patient survival across independent cohorts. MCM7 emerged as a central senescence-associated driver. ScRNA-seq and mIF confirmed MCM7 characterizes a highly proliferative, clonally expanding subset of CD8+ T cells within the tumor microenvironment. In vitro, MCM7 knockdown significantly inhibited HepG2 cell proliferation and upregulated senescence enforcers p16 and p21, whereas overexpression facilitated evasion. Additionally, TIDE analysis revealed that high-risk patients exhibited elevated immune evasion potential, predicting poor immunotherapy response.
CONCLUSION: This integrative multi-omics framework uncovers an MCM7 MCM7-driven senescence-associated axis promising HCC progression and immune dysfunction, offering a robust tool for prognostic stratification and novel therapeutic insights.
PMID:42183188 | PMC:PMC13195000 | DOI:10.3389/fimmu.2026.1762222
A pathogen lncRNA secreted into rice sequesters a host miRNA for virulence
Nature, Published online: 20 May 2026; doi:10.1038/s41586-026-10572-x
A fungal long non-coding RNA from Magnaporthe oryzae translocates into rice cells to sequester a host microRNA that normally represses PKR1, a negative immunity regulator, thereby facilitating infection and revealing a widespread RNA-based pathogen–host interaction mechanism.High-salt diet in macrophage-associated metabolic disorders: Mechanisms and therapeutic implications
Chin Med J (Engl). 2026 May 19. doi: 10.1097/CM9.0000000000004098. Online ahead of print.
ABSTRACT
High-salt diet (HSD) has emerged as a prevalent environmental factor that exacerbates chronic inflammation and insulin resistance in obesity-associated type 2 diabetes (T2D) by modulating macrophage polarization, metabolic reprogramming, and epigenetic imprinting. Current evidence demonstrates that HSD activates p38/mitogen-activated protein kinase (MAPK), nuclear factor kappa-B (NF-κB), and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome signaling pathways, by which it drives macrophage polarization toward a proinflammatory M1 phenotype while inducing a glycolysis-dominant metabolic shift, thereby establishing a persistent "metabolic memory". Moreover, HSD orchestrates metabolic memory in macrophages through coordinated epigenetic machinery, including histone modifications (Trimethylation of histone H3 at lysine 4 [H3K4me3] and Acetylation of histone H3 at lysine 27 [H3K27ac]), DNA methylation, and noncoding RNAs (e.g., long non-coding RNA MALAT1 and miR-155), leading to sustained inflammatory phenotypes. In multiple metabolic organs (e.g., adipose tissue, liver, pancreas, and gut), the HSD-macrophage axis aggravates systemic insulin resistance through shared proinflammatory signaling and other tissue-specific mechanisms. Most importantly, therapeutic strategies targeting the NLRP3 inflammasome, metabolic pathways, and epigenetic alterations offer novel approaches for managing metabolic inflammation. Future investigations are encouraged to leverage lineage tracing, single-cell sequencing, and spatial multi-omics technologies to advance the development of precision medicine for macrophage-associated metabolic disorders.
PMID:42156155 | DOI:10.1097/CM9.0000000000004098
Imaging interface-controlled bulk oxygen spillover
Nature, Published online: 15 April 2026; doi:10.1038/s41586-026-10324-x
In situ microscopic single-particle imaging demonstrates the significance of rationally engineered metal–support interfaces for activating the oxygen in bulk catalyst, helping elucidate reaction pathways in catalytic conversions.