Supplementary Tables S1-S14 from Mutational Signatures and Clonal Hematopoiesis in Intestinal Metaplasia across Countries with Varying Stomach Cancer Incidence

Supplementary Table S1 details all IM and control samples with associated profiling platforms, including targeted DNA sequencing, WGS, single-cell RNA-seq, bulk RNA-seq, shotgun metagenomics, EM-seq, and Stereo-seq datasets. Supplementary Table S2 summarizes major genomic and molecular findings across different countries and ancestral backgrounds. Supplementary Table S3 lists significantly mutated genes identified in non-hypermutated intestinal metaplasia samples. Supplementary Table S4 shows pathways up-regulated in intestinal lineage cells exhibiting high KRAS/ERK expression. Supplementary Table S5 provides a catalog of established IM and normal gastric organoid lines with relevant metadata. Supplementary Table S6 reports Hallmark and GO pathway enrichment analyses comparing KRAS/MAPK-mutated versus wild-type IM, and severe versus mild IM organoids. Supplementary Table S7 displays country- and risk-group-specific proportions of SBS mutational signatures derived from targeted panel sequencing. Supplementary Table S8 shows correlations between mutational signature exposures and patient age in IM samples, including significance from Pearson’s and Spearman’s tests with and without outliers. Supplementary Table S9 lists germline variants occurring in known somatic driver genes among IM patients. Supplementary Table S10 summarizes univariate and multivariate logistic regression analyses linking clinical and molecular risk factors to dysplasia and early gastric neoplasia. Supplementary Table S11 shows associations between bacterial genera abundance and PIGR mutational status in IM samples. Supplementary Table S12 profiles the composition of the oral microbiome from saliva samples of IM patients. Supplementary Table S13 lists Seahorse mitochondrial stress test instrument parameters and assay conditions. Supplementary Table S14 provides Seahorse mitochondrial stress test settings specific to DCA treatment experiments.

补充表S1详述了所有肠上皮化生（intestinal metaplasia, IM）及对照样本的相关组学分析平台，涵盖靶向DNA测序、全基因组测序（Whole Genome Sequencing, WGS）、单细胞RNA测序（single-cell RNA-seq）、批量RNA测序（bulk RNA-seq）、鸟枪宏基因组学、EM-seq以及Stereo-seq数据集。补充表S2汇总了不同国家及祖先背景下的主要基因组与分子发现。补充表S3列出了非高突变型肠上皮化生样本中鉴定出的显著突变基因。补充表S4展示了KRAS/ERK高表达肠道谱系细胞中上调的通路。补充表S5提供了已建立的肠上皮化生及正常胃类器官系的相关元数据（metadata）。补充表S6报告了针对KRAS/MAPK突变型与野生型肠上皮化生、重度与轻度肠上皮化生类器官的Hallmark通路及基因本体（Gene Ontology, GO）富集分析结果。补充表S7展示了基于靶向测序面板得到的、按国家及风险分组划分的单碱基替换（Single Base Substitution, SBS）突变特征比例。补充表S8展示了肠上皮化生样本中突变特征暴露度与患者年龄的相关性，包含去除异常值与未去除异常值情况下Pearson检验及Spearman检验的显著性结果。补充表S9列出了肠上皮化生患者已知体细胞驱动基因中存在的种系变异。补充表S10汇总了将临床与分子风险因素与异型增生及早期胃肿瘤相关联的单变量与多变量logistic回归分析结果。补充表S11展示了肠上皮化生样本中细菌属丰度与PIGR突变状态之间的关联。补充表S12分析了肠上皮化生患者唾液样本的口腔微生物组组成。补充表S13列出了Seahorse线粒体压力测试的仪器参数与实验条件。补充表S14提供了针对脱氧胆酸（deoxycholic acid, DCA）处理实验的Seahorse线粒体压力测试专属设置。