Q-omics provides the consensus-scored CDH5 profile across patient tissues and cancer cell-line models. CDH5 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CDH5 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, CDH5 protein abundance shows 25,958 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, and LSCC as cancer lineages where CDH5 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 CDH5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CDH5 survival associations across molecular data types. CDH5 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (7) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CDH5 RNA expression–survival associations across cancer types. High CDH5 expression shows unfavorable associations in KIRP, UVM and MESO, but favorable associations in KIRC, HNSC and UCS. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for CDH5 RNA expression.
This table summarizes CDH5 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CDH5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CDH5 shows lower tumor expression in LUAD, LUSC, KIRP and KICH and higher tumor expression in KIRC and HNSC. The KIRC box plot shows higher CDH5 RNA expression in tumor versus normal tissue (log2 FC = +1.752, t-test p < 0.001).
This table shows molecular features associated with CDH5 in patient tissues and cancer cell lines. In patient samples, CDH5 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, CDH5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BREAST and LARGE_INTESTINE.
