Q-omics provides the consensus-scored VRK3 profile across patient tissues and cancer cell-line models. VRK3 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, VRK3 is differentially expressed in 11, with the highest sampling consensus in THCA. Additionally, VRK3 RNA expression shows 19,975 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, THCA, and ACC as cancer lineages where VRK3 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 VRK3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VRK3 survival associations across molecular data types. VRK3 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (3) 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 VRK3 RNA expression–survival associations across cancer types. High VRK3 expression shows unfavorable associations in LGG, ACC and LUSC, but favorable associations in KIRC, SCLC and THYM. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for VRK3 RNA expression.
This table summarizes VRK3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 5. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for VRK3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VRK3 shows lower tumor expression in THCA and KICH and higher tumor expression in KIRC, STAD, LIHC and HNSC. The THCA box plot shows higher VRK3 RNA expression in normal versus tumor tissue (log2 FC = −0.387, t-test p < 0.001).
This table shows molecular features associated with VRK3 in patient tissues and cancer cell lines. In patient samples, VRK3 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, VRK3 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 UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
