Q-omics provides the consensus-scored VCAN profile across patient tissues and cancer cell-line models. VCAN expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, VCAN is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, VCAN protein abundance shows 25,763 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight MESO, KIRC, and PDAC as cancer lineages where VCAN 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 VCAN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VCAN survival associations across molecular data types. VCAN RNA expression shows survival associations in the most cancer types (22), followed by mutation status (12) 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 VCAN RNA expression–survival associations across cancer types. High VCAN expression shows unfavorable associations in MESO, STAD, UVM and BLCA, but favorable associations in UCS and LGG. 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 VCAN RNA expression.
This table summarizes VCAN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 8. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for VCAN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VCAN shows higher tumor expression in KIRC, HNSC, STAD, COAD, KIRP and LUAD. The KIRC box plot shows higher VCAN RNA expression in tumor versus normal tissue (log2 FC = +2.554, t-test p < 0.001).
This table shows molecular features associated with VCAN in patient tissues and cancer cell lines. In patient samples, VCAN 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, VCAN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in BONE and LARGE_INTESTINE.
