Q-omics provides the consensus-scored VCP profile across patient tissues and cancer cell-line models. VCP expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, VCP is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, VCP RNA expression shows 18,618 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight LUAD, HNSC, and ACC as cancer lineages where VCP 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 VCP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VCP survival associations across molecular data types. VCP RNA expression shows survival associations in the most cancer types (21), 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 VCP RNA expression–survival associations across cancer types. High VCP expression shows unfavorable associations in LUAD, UVM, ACC and MESO, but favorable associations in KIRC and SCLC. The LUAD 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 LUAD as the clearest survival context for VCP RNA expression.
This table summarizes VCP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for VCP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VCP shows higher tumor expression in HNSC, COAD, BLCA, LIHC, STAD and LUSC. The HNSC box plot shows higher VCP RNA expression in tumor versus normal tissue (log2 FC = +0.676, t-test p < 0.001).
This table shows molecular features associated with VCP in patient tissues and cancer cell lines. In patient samples, VCP shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, VCP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in OVARY and UPPER_AERODIGESTIVE_TRACT.
