ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2026
Mapping the genetic landscape of hereditary diffuse-type gastric cancer progression.
Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The interplay of the microbiome, host genetics, and epigenetic modifications in gastric cancer.Frontiers in microbiology · 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
11 authors.
Funding
Abstract
backgroundHereditary diffuse gastric cancer (HDGC), caused by pathogenic variants (PVs) in CDH1, typically presents as early-stage mucosal lesions composed of non-proliferative signet ring cells (SRCs). While loss of E-cadherin initiates tumorigenesis, the somatic genetic alterations driving progression to advanced disease remain poorly understood.
objectiveOur goal was to identify morphological and genetic changes associated with HDGC progression.
designWe performed whole exome sequencing on 38 gastric tumors from 26 HDGC patients, spanning early to advanced stages, and compared genetic alterations across tumor stages.
resultsEarly-stage HDGC lesions exhibited minimal somatic alterations, with low tumor mutational burden (TMB) and few cancer-related mutations. In contrast, advanced tumors showed a significant increase in TMB and frequent somatic mutations in CDH1, TP53, and genes involved in TGF-β signaling, cell adhesion, and actomyosin contractility (e.g., SMAD4, FAT4, RHOA). Copy number variations (CNVs) were also more prevalent in advanced tumors, including recurrent loss of 3p and 17p and amplification of oncogenes MYC and MET. CNV profiles varied between tumor regions, indicating intratumoral heterogeneity and potential clonal evolution.
conclusionHDGC progression is marked by a stepwise accumulation of somatic mutations and chromosomal alterations. While early lesions remain genetically quiet, advanced tumors exhibit complex genetic landscapes, including CDH1 inactivation, oncogenic mutations, and CNVs. These findings highlight key molecular events in HDGC progression and may inform future strategies for early detection and targeted intervention.
Indexed as
Identifiers
What Socratic 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 Socratic graph.