ArticleCommunications biology2026
Divergent clonal evolution and tumor microenvironment remodeling shape gastric cancer peritoneal metastasis.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Gastric cancer peritoneal metastasis (GCPM) is a distinct clinical entity with a poor prognosis, characterized by aggressive features and limited treatment options. Understanding its molecular biology is critical for developing effective therapies. We performed whole genome and transcriptome sequencing on GCPM samples and partially paired primary gastric cancer (GC) tissues from 14 and 26 patients, respectively. Our analysis reveals substantial intra-patient heterogeneity between GCPM and primary tumors at both genetic and functional levels. Inter-patient variability is observed in mutational overlaps, with some signatures unique to either GCPM or primary tumors. Tumor evolution analysis suggests divergent clonal evolution, with distinct clones specific to GCPM or primary tumors in most patients. Transcriptomic profile reveals a high heterogeneity in the primary tumors, with five tumors presenting GCPM characteristics. The tumor microenvironment (TME) is poorly conserved between primary GC and GCPM, with desert-type primary tumors often transitioning to immune-enriched TMEs in metastases. These findings suggest that immunotherapy resistance in GCPM may arise from factors beyond intrinsic TME characteristics, such as limited drug delivery due to the peritoneal-plasma barrier. Collectively, our results highlight significant molecular and TME heterogeneity between GCPM and primary tumors, emphasizing the need for GCPM-specific stratification and innovative treatment strategies to improve outcomes.
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.