Q-omics provides the consensus-scored CDON profile across patient tissues and cancer cell-line models. CDON expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, CDON is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, CDON RNA expression shows 19,951 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight BLCA, KIRC, and UVM as cancer lineages where CDON 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 CDON — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CDON survival associations across molecular data types. CDON RNA expression shows survival associations in the most cancer types (26), followed by mutation status (9) 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 CDON RNA expression–survival associations across cancer types. High CDON expression shows unfavorable associations in BLCA, KIRP, ACC and KICH, but favorable associations in UCS and BRCA. The BLCA Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .003). Together, the overview and detailed table identify BLCA as the clearest survival context for CDON RNA expression.
This table summarizes CDON 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 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CDON. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CDON shows lower tumor expression in THCA, BLCA, LUAD, UCEC and BRCA and higher tumor expression in KIRC. The KIRC box plot shows higher CDON RNA expression in tumor versus normal tissue (log2 FC = +1.775, t-test p < 0.001).
This table shows molecular features associated with CDON in patient tissues and cancer cell lines. In patient samples, CDON shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, CDON 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 URINARY_TRACT and LARGE_INTESTINE.
