Q-omics provides the consensus-scored VTN profile across patient tissues and cancer cell-line models. VTN expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, VTN is differentially expressed in 12, with the highest sampling consensus in LUAD. Additionally, VTN protein abundance shows 28,979 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, LUAD, and GBM as cancer lineages where VTN 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 VTN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VTN survival associations across molecular data types. VTN RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3) and mass-spec protein abundance (13). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible VTN RNA expression–survival associations across cancer types. High VTN expression shows unfavorable associations in KIRP, LUSC, UVM, KIRC and STAD, but favorable associations in LIHC. The KIRP 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 KIRP as the clearest survival context for VTN RNA expression.
This table summarizes VTN 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 10. The strongest signals are observed in LUAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for VTN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VTN shows lower tumor expression in LUAD, KICH, BLCA, UCEC, LUSC and THCA. The LUAD box plot shows higher VTN RNA expression in normal versus tumor tissue (log2 FC = −1.522, t-test p < 0.001).
This table shows molecular features associated with VTN in patient tissues and cancer cell lines. In patient samples, VTN 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, VTN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in CNS and SOFT_TISSUE.
