Q-omics provides the consensus-scored CDH2 profile across patient tissues and cancer cell-line models. CDH2 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, CDH2 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, CDH2 RNA expression shows 18,593 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight MESO, KIRC, and KIRP as cancer lineages where CDH2 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 CDH2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CDH2 survival associations across molecular data types. CDH2 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (8) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CDH2 RNA expression–survival associations across cancer types. High CDH2 expression shows unfavorable associations in MESO, STAD, BLCA and ACC, but favorable associations in KIRC and OV. 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 CDH2 RNA expression.
This table summarizes CDH2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for CDH2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CDH2 shows lower tumor expression in KICH and higher tumor expression in KIRC, BRCA, HNSC, THCA and LUAD. The KIRC box plot shows higher CDH2 RNA expression in tumor versus normal tissue (log2 FC = +1.697, t-test p < 0.001).
This table shows molecular features associated with CDH2 in patient tissues and cancer cell lines. In patient samples, CDH2 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, CDH2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BONE.
