Q-omics provides the consensus-scored VHL profile across patient tissues and cancer cell-line models. VHL expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, VHL is differentially expressed in 15, with the highest sampling consensus in BLCA. Additionally, VHL protein abundance shows 24,646 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight ACC, BLCA, and PDAC as cancer lineages where VHL 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 VHL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VHL survival associations across molecular data types. VHL RNA expression shows survival associations in the most cancer types (27), followed by mutation status (1) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible VHL RNA expression–survival associations across cancer types. High VHL expression shows unfavorable associations in ACC, MESO, KICH and LIHC, but favorable associations in SCLC and READ. The ACC 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 ACC as the clearest survival context for VHL RNA expression.
This table summarizes VHL 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 BLCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for VHL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VHL shows lower tumor expression in THCA and KIRC and higher tumor expression in BLCA, COAD, STAD and LUAD. The BLCA box plot shows higher VHL RNA expression in tumor versus normal tissue (log2 FC = +1.438, t-test p < 0.001).
This table shows molecular features associated with VHL in patient tissues and cancer cell lines. In patient samples, VHL 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, VHL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and UPPER_AERODIGESTIVE_TRACT.
