Q-omics provides the consensus-scored PML profile across patient tissues and cancer cell-line models. PML expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PML is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, PML protein abundance shows 23,394 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight UVM, HNSC, and PDAC as cancer lineages where PML 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 PML — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PML survival associations across molecular data types. PML RNA expression shows survival associations in the most cancer types (24), followed by mutation status (6) 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 PML RNA expression–survival associations across cancer types. High PML expression shows unfavorable associations in PAAD, MESO, UCEC and LGG, but favorable associations in UVM and SKCM. The UVM Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify UVM as the clearest survival context for PML RNA expression.
This table summarizes PML tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PML. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PML shows higher tumor expression in HNSC, KIRC, COAD, KIRP, LIHC and THCA. The HNSC box plot shows higher PML RNA expression in tumor versus normal tissue (log2 FC = +1.382, t-test p < 0.001).
This table shows molecular features associated with PML in patient tissues and cancer cell lines. In patient samples, PML 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, PML 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 LUNG_SCLC and BREAST.
