Q-omics provides the consensus-scored CPM profile across patient tissues and cancer cell-line models. CPM expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in UCEC. Among the 18 cancer types available for tumor–normal comparison, CPM is differentially expressed in 10, with the highest sampling consensus in KICH. Additionally, CPM protein abundance shows 23,282 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UCEC, KICH, and LSCC as cancer lineages where CPM 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 CPM — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CPM survival associations across molecular data types. CPM RNA expression shows survival associations in the most cancer types (20), followed by mutation status (4) 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 CPM RNA expression–survival associations across cancer types. High CPM expression shows unfavorable associations in LGG, UVM, STAD and BLCA, but favorable associations in UCEC and KIRC. The UCEC 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 UCEC as the clearest survival context for CPM RNA expression.
This table summarizes CPM tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 7. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CPM. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CPM shows lower tumor expression in KICH, COAD, KIRC, LUSC and LUAD and higher tumor expression in THCA. The KICH box plot shows higher CPM RNA expression in normal versus tumor tissue (log2 FC = −4.346, t-test p < 0.001).
This table shows molecular features associated with CPM in patient tissues and cancer cell lines. In patient samples, CPM shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, CPM RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and BONE.
