Q-omics provides the consensus-scored CANX profile across patient tissues and cancer cell-line models. CANX expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CANX is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, CANX protein abundance shows 20,376 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, and PDAC as cancer lineages where CANX 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 CANX — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CANX survival associations across molecular data types. CANX RNA expression shows survival associations in the most cancer types (22), followed by mutation status (5) 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 CANX RNA expression–survival associations across cancer types. High CANX expression shows unfavorable associations in UVM, KICH, HNSC, CESC and KIRP, but favorable associations in KIRC. 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 CANX RNA expression.
This table summarizes CANX 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 9. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CANX. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CANX shows lower tumor expression in THCA and higher tumor expression in KIRC, LIHC, STAD, COAD and HNSC. The KIRC box plot shows higher CANX RNA expression in tumor versus normal tissue (log2 FC = +1.008, t-test p < 0.001).
This table shows molecular features associated with CANX in patient tissues and cancer cell lines. In patient samples, CANX shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, CANX RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Myeloma, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and UPPER_AERODIGESTIVE_TRACT.
