Q-omics provides the consensus-scored MVK profile across patient tissues and cancer cell-line models. MVK expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, MVK is differentially expressed in 11, with the highest sampling consensus in KICH. Additionally, MVK protein abundance shows 27,037 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight MESO, KICH, and GBM as cancer lineages where MVK 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 MVK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MVK survival associations across molecular data types. MVK RNA expression shows survival associations in the most cancer types (21), followed by mutation status (2) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MVK RNA expression–survival associations across cancer types. High MVK expression shows unfavorable associations in MESO, KICH, OV, SKCM and LIHC, but favorable associations in KIRP. The MESO 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 MESO as the clearest survival context for MVK RNA expression.
This table summarizes MVK 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 7. The strongest signals are observed in BLCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MVK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MVK shows lower tumor expression in KICH, LUAD and THCA and higher tumor expression in BLCA, COAD and UCEC. The KICH box plot shows higher MVK RNA expression in normal versus tumor tissue (log2 FC = −1.521, t-test p < 0.001).
This table shows molecular features associated with MVK in patient tissues and cancer cell lines. In patient samples, MVK 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, MVK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BREAST.
