Q-omics provides the consensus-scored VDR profile across patient tissues and cancer cell-line models. VDR expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, VDR is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, VDR RNA expression shows 22,242 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UVM, KIRC, and GBM as cancer lineages where VDR 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 VDR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VDR survival associations across molecular data types. VDR RNA expression shows survival associations in the most cancer types (24), followed by mutation status (9) 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 VDR RNA expression–survival associations across cancer types. High VDR expression shows unfavorable associations in UVM, LGG, PAAD, LAML and LUSC, but favorable associations in ESCA. The UVM Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify UVM as the clearest survival context for VDR RNA expression.
This table summarizes VDR 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 6. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for VDR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VDR shows lower tumor expression in KIRC and KIRP and higher tumor expression in HNSC, STAD, LUAD and UCEC. The KIRC box plot shows higher VDR RNA expression in normal versus tumor tissue (log2 FC = −1.554, t-test p < 0.001).
This table shows molecular features associated with VDR in patient tissues and cancer cell lines. In patient samples, VDR shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, VDR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BONE.
