ArticleFrontiers in immunology2026
Multi-omics profiling of sodium-overload (NECSO) programs identifies NEK8 as a central driver of colorectal cancer progression through single-cell and spatial transcriptomics.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Article
- Metal-dependent regulated cell death: Molecular architecture and translational frontiers.iMeta · 2026Review
- Mechanistic roles and clinical applications of tertiary lymphoid structures in colorectal cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Colorectal cancer (CRC) is a leading cause of cancer-related death, often marked by intratumoral heterogeneity, immune evasion, and therapeutic resistance. Recent advancements in single-cell and spatial transcriptomics have enabled a deeper understanding of the tumor microenvironment (TME), revealing key insights into metabolic reprogramming and immune suppression. This study focuses on the role of sodium-overload cell death (NECSO) and its interaction with immune modulation in CRC pathogenesis. Methods: We employed an integrated multi-omic approach combining single-cell RNA-sequencing (scRNA-seq) and spatial transcriptomics (ST) to identify key NECSO-related genes in CRC. Through differential expression analysis and LASSO-Cox regression modeling, we developed a NECSO-based prognostic model. We validated our findings using TCGA and GEO datasets, assessing immune infiltration and spatial gene localization to determine the relationship between NEK8 and immune modulation. Results: Our NECSO-derived five-gene signature (NEK8, DRD4, EPHB2, CYTH2, ACOT11) effectively stratified CRC patients into high- and low-risk groups. High-risk patients exhibited reduced immune cell infiltration, particularly CD8 Conclusions: The NECSO-derived signature provides a novel prognostic tool that integrates immune evasion and metabolic reprogramming in CRC. NEK8 plays a pivotal role in shaping the immune landscape and could serve as a biomarker for immunotherapy response, offering a pathway for personalized treatment strategies in precision oncology.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.