Q-omics provides the consensus-scored CDH11 profile across patient tissues and cancer cell-line models. CDH11 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CDH11 is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, CDH11 protein abundance shows 22,138 significant protein co-abundance associations, with the highest sampling consensus in UCEC. Together, these results highlight KIRP, HNSC, and UCEC as cancer lineages where CDH11 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 CDH11 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CDH11 survival associations across molecular data types. CDH11 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CDH11 RNA expression–survival associations across cancer types. High CDH11 expression shows unfavorable associations in KIRP, BLCA, STAD, LGG and ACC, but favorable associations in UCS. The KIRP 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 KIRP as the clearest survival context for CDH11 RNA expression.
This table summarizes CDH11 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 5. The strongest signals are observed in HNSC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for CDH11. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CDH11 shows lower tumor expression in KICH and higher tumor expression in HNSC, KIRC, COAD, BRCA and STAD. The HNSC box plot shows higher CDH11 RNA expression in tumor versus normal tissue (log2 FC = +2.907, t-test p < 0.001).
This table shows molecular features associated with CDH11 in patient tissues and cancer cell lines. In patient samples, CDH11 shows the broadest associations at the RNA and protein expression levels, with UCEC recurring as the lineage with the largest associated feature set. In cancer cell lines, CDH11 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and LARGE_INTESTINE.
