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Molecular features of early- vs. late-onset gastric cancer: a systematic review and meta-analysis

BMC Cancer. 2026 Jan 14. doi: 10.1186/s12885-026-15567-5. Online ahead of print.

ABSTRACT

BACKGROUND: Early-onset gastric cancer (EOGC), diagnosed before age 50, is characterized by distinct clinicopathological features, though its molecular landscape remains poorly defined.

METHODS: A systematic literature search of PubMed, Embase, and Web of Science identified studies comparing molecular characteristics of EOGC and late-onset gastric cancer (LOGC). Meta-analyses assessed differences in The Cancer Genome Atlas (TCGA) molecular subtypes, gene mutations, therapeutic biomarkers, and serum tumor markers. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated; heterogeneity was assessed using the I2 statistic.

RESULTS: EOGC was associated with a higher prevalence of the genomically stable (GS) subtype (OR = 1.71, 95% CI: 1.37-2.12) and a lower prevalence of the chromosomal instability (CIN) subtype (OR = 0.62, 95% CI: 0.50-0.77). CDH1 mutations were more frequent in EOGC (OR = 3.44, 95% CI: 2.85-4.16), while HER2 expression (OR = 0.54, 95% CI: 0.43-0.67), dMMR/MSI-H status (OR = 0.25, 95% CI: 0.12-0.53), and p53 expression (OR = 0.56, 95% CI: 0.39-0.82) were significantly lower. Serum markers including CEA and CA19-9 were also less frequently elevated in EOGC.

CONCLUSION: EOGC represents a biologically distinct subset of gastric cancer with unique genomic and immunological features. These findings support age-specific diagnostic approaches and emphasize the value of multiomic strategies to uncover the mechanisms driving early-onset disease.

PMID:41535782 | DOI:10.1186/s12885-026-15567-5

Multi-omics to study chronic respiratory diseases and viral infections

Eur Respir Rev. 2026 Jan 14;35(179):240286. doi: 10.1183/16000617.0286-2024. Print 2026 Jan.

ABSTRACT

Despite recent advances, the underlying mechanisms of the development and progression of many chronic respiratory diseases remain to be elucidated. Factors such as heterogeneity and complexity of human diseases and difficulty interpreting large datasets hinder research into chronic respiratory diseases. Omics assesses the changes in specific biological entities, such as mRNA expression, epigenetics/epigenomics, genomics, proteomics, metagenomics and metabolomics, and provides valuable insights into the roles of these processes in chronic respiratory diseases. High-throughput omics at bulk, single-cell and spatial levels empower the exploration of disease-related changes through untargeted data-driven statistical methods. Multi-omics is the exploration and integration of multiple biological processes, which compared to a single-omics, can provide a substantially greater and more holistic overview of the pathogenic mechanisms that underpin complex diseases. Multi-omics analysis can comprehensively characterise the mechanisms that drive chronic respiratory diseases, capturing unique biological signatures and cellular interactions at different omics levels. Use of these methods has begun to identify key factors and biomarkers in chronic respiratory diseases. Here, we review current omics approaches and highlight recent advances in respiratory research achieved using multi-omics and integrative methods. Our review provides a valuable resource for researchers and clinicians in this area.

PMID:41534886 | DOI:10.1183/16000617.0286-2024

Extrachromosomal DNA replication and maintenance couple with DNA damage pathway in tumors

This study demonstrates that extrachromosomal DNA (ecDNA) replication induces DNA double-strand breaks and activates the DNA damage response (DDR). The DDR pathways, such as alt-NHEJ, are critical for ecDNA maintenance in tumor cells. Mechanistic insights into ecDNA replication and maintenance unveil a therapeutic approach for treating tumors harboring ecDNA.

ZNF655 accelerates progression of pancreatic cancer by promoting the binding of E2F1 and CDK1

Oncogenesis, Published online: 04 August 2022; doi:10.1038/s41389-022-00418-2

ZNF655 accelerates progression of pancreatic cancer by promoting the binding of E2F1 and CDK1
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