Q-omics provides the consensus-scored VCL profile across patient tissues and cancer cell-line models. VCL expression is associated with patient survival in 31 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, VCL is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, VCL protein abundance shows 31,449 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight MESO, HNSC, and PDAC as cancer lineages where VCL 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 VCL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VCL survival associations across molecular data types. VCL RNA expression shows survival associations in the most cancer types (31), followed by mutation status (4) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible VCL RNA expression–survival associations across cancer types. High VCL expression shows unfavorable associations in MESO, BLCA, KICH, PAAD and UVM, but favorable associations in KIRC. 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 VCL RNA expression.
This table summarizes VCL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for VCL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VCL shows lower tumor expression in KIRC, KICH, BLCA and UCEC and higher tumor expression in HNSC and LIHC. The HNSC box plot shows higher VCL RNA expression in tumor versus normal tissue (log2 FC = +0.839, t-test p < 0.001).
This table shows molecular features associated with VCL in patient tissues and cancer cell lines. In patient samples, VCL 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, VCL 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 LARGE_INTESTINE and BONE.
