Q-omics provides the consensus-scored VENTX profile across patient tissues and cancer cell-line models. VENTX expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, VENTX is differentially expressed in 13, with the highest sampling consensus in COAD. Additionally, VENTX RNA expression shows 22,527 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, COAD, and GBM as cancer lineages where VENTX 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 VENTX — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes VENTX survival associations across molecular data types. VENTX RNA expression shows survival associations in the most cancer types (26), followed by mutation status (7) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible VENTX RNA expression–survival associations across cancer types. High VENTX expression shows unfavorable associations in KIRC, LGG, OV and GBM, but favorable associations in SKCM and KIRP. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify KIRC as the clearest survival context for VENTX RNA expression.
This table summarizes VENTX tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for VENTX. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. VENTX shows lower tumor expression in LUSC, UCEC and BRCA and higher tumor expression in COAD, KIRC and THCA. The COAD box plot shows higher VENTX RNA expression in tumor versus normal tissue (log2 FC = +1.712, t-test p < 0.001).
This table shows molecular features associated with VENTX in patient tissues and cancer cell lines. In patient samples, VENTX 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, VENTX RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and SOFT_TISSUE.
