Q-omics provides the consensus-scored PKM profile across patient tissues and cancer cell-line models. PKM expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PKM is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, PKM protein abundance shows 30,827 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight UVM, HNSC, and PDAC as cancer lineages where PKM 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 PKM — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PKM survival associations across molecular data types. PKM RNA expression shows survival associations in the most cancer types (25), followed by mutation status (2) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PKM RNA expression–survival associations across cancer types. High PKM expression shows unfavorable associations in UVM, MESO, HNSC, KICH, PAAD and LIHC. 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 PKM RNA expression.
This table summarizes PKM tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PKM. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PKM shows higher tumor expression in HNSC, COAD, KIRC, KIRP, STAD and LUAD. The HNSC box plot shows higher PKM RNA expression in tumor versus normal tissue (log2 FC = +1.693, t-test p < 0.001).
This table shows molecular features associated with PKM in patient tissues and cancer cell lines. In patient samples, PKM 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, PKM RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in CNS and BONE.
