Q-omics provides the consensus-scored PMVK profile across patient tissues and cancer cell-line models. PMVK expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PMVK is differentially expressed in 9, with the highest sampling consensus in LIHC. Additionally, PMVK protein abundance shows 22,837 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight UVM, LIHC, and PDAC as cancer lineages where PMVK 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 PMVK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PMVK survival associations across molecular data types. PMVK RNA expression shows survival associations in the most cancer types (21), followed by mutation status (1) 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 PMVK RNA expression–survival associations across cancer types. High PMVK expression shows unfavorable associations in UVM, ACC, KICH and LAML, but favorable associations in OV and MESO. The UVM 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 UVM as the clearest survival context for PMVK RNA expression.
This table summarizes PMVK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 6. The strongest signals are observed in LIHC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PMVK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PMVK shows lower tumor expression in KICH and THCA and higher tumor expression in LIHC, KIRC, BRCA and CHOL. The LIHC box plot shows higher PMVK RNA expression in tumor versus normal tissue (log2 FC = +1.482, t-test p < 0.001).
This table shows molecular features associated with PMVK in patient tissues and cancer cell lines. In patient samples, PMVK shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, PMVK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BREAST and UPPER_AERODIGESTIVE_TRACT.
