Q-omics provides the consensus-scored CDH10 profile across patient tissues and cancer cell-line models. CDH10 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, CDH10 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, CDH10 RNA expression shows 12,873 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight MESO, KIRC, and TGCT as cancer lineages where CDH10 shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for CDH10 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CDH10 survival associations across molecular data types. CDH10 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (8) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CDH10 RNA expression–survival associations across cancer types. High CDH10 expression shows unfavorable associations in MESO, KIRP, BLCA, BRCA, KICH and ACC. The MESO Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify MESO as the clearest survival context for CDH10 RNA expression.
This table summarizes CDH10 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for CDH10. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CDH10 shows lower tumor expression in KIRC, COAD, KIRP, LUAD, BLCA and READ. The KIRC box plot shows higher CDH10 RNA expression in normal versus tumor tissue (log2 FC = −0.227, t-test p < 0.001).
This table shows molecular features associated with CDH10 in patient tissues and cancer cell lines. In patient samples, CDH10 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, CDH10 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUSC and LARGE_INTESTINE.
