Aug 2026· iScience· Vol 29, pp. 116913· 0 citations· 156 references
Medicine
TL;DR
Studies investigating the gastritis-to-carcinoma sequence using genomics, epigenomics, transcriptomics, proteomics, metabolomics, and microbiome analyses provide valuable insights into gastric carcinogenesis while highlighting the need for cautious interpretation and translational validation.
Abstract
Summary The progression from chronic gastritis to gastric cancer is a complex and multistep process. Early detection of this transition is critical for improving patient survival; however, the underlying molecular mechanisms remain incompletely understood. Recent advances in multi-omics technologies have provided powerful tools for high-resolution characterization of disease-associated molecular alterations. In this review, we summarize studies investigating the gastritis-to-carcinoma sequence using genomics, epigenomics, transcriptomics, proteomics, metabolomics, and microbiome analyses. Particular emphasis is placed on evidence from human cohorts, single-cell sequencing, and spatial transcriptomics, which have helped characterize cellular heterogeneity, immune microenvironment remodeling, and cell-cell interactions. We also discuss the role of the microbiome, particularly Helicobacter pylori, in disease progression. Integration of these multi-layered datasets can generate mechanistic hypotheses and candidate biomarkers, but most findings require independent validation before clinical implementation. Overall, multi-omics approaches provide valuable insights into gastric carcinogenesis while highlighting the need for cautious interpretation and translational validation.
This study provides a systematic multi-omics characterization of immune microenvironment remodelling in CRC and identifies candidate molecular regulators that may serve as potential targets for future immunotherapy research.
Hong-Wei Zeng, Lie-Wen Lin, Yumei Chen et al.· Cancer Genomics & Proteomics· 0 citations
Background: Small-cell lung cancer (SCLC) is a rare but highly aggressive malignancy defined by rapid progression, early metastasis, and profound therapeutic resistance. Its extensive heterogeneity across genomic, transcriptomic, epigenetic, proteomic, and microenvironmental levels continues to undermine precision medi...
Saman Zeeshan, Caila McVey, Shafaq Majeed et al.· Cancers· 0 citations
This work discusses the assumptions and sampling biases that constrain phylogenetic inference, the causal limits of cross-sectional tumor atlases, clonal hematopoiesis, and the incremental value of broad multi-omics over focused assays.
Wen-Yi Fan, Chun-Hong Zheng· Frontiers in Oncology· 0 citations
The findings provide a system-level framework describing the associations between dysbiosis-relevant host pathways, CRC-related regulatory networks, and immune responses and represent hypothesis-generating host candidates for further mechanistic and clinical validation.
Huda Altoukhi, Nawal H. Siddig, N. Al-Hoshani et al.· Journal of Clinical Medicine· 0 citations
Malignant pleural mesothelioma (MPM) exhibits substantial molecular and cell-state heterogeneity, together with marked spatial variation in its immune and stromal microenvironment. Histological classification and individual biomarkers alone cannot adequately explain its evolution or heterogeneous treatment responses. T...
Hongmei Li, Kunzhong Zhou, Ruiting Xu et al.· Frontiers in Oncology· 0 citations
Patient-derived organoids (PDOs) are widely used platforms for cancer modeling and precision oncology because they preserve patient-specific genetic backgrounds, recapitulate aspects of native tissue architecture, and allow long-term expansion, repeated functional interrogation, and drug screening. Accordingly, multi-o...
J. Lim, Yeju Kim, Jin-Ku Lee· Organoid· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.