Q-omics provides the consensus-scored CPZ profile across patient tissues and cancer cell-line models. CPZ expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CPZ is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, CPZ protein abundance shows 19,332 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, HNSC, and LSCC as cancer lineages where CPZ 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 CPZ — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CPZ survival associations across molecular data types. CPZ RNA expression shows survival associations in the most cancer types (24), followed by mutation status (9) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CPZ RNA expression–survival associations across cancer types. High CPZ expression shows unfavorable associations in KIRP, KIRC, THCA and OV, but favorable associations in UCEC and LAML. The KIRP 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 KIRP as the clearest survival context for CPZ RNA expression.
This table summarizes CPZ 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 8. The strongest signals are observed in HNSC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for CPZ. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CPZ shows lower tumor expression in UCEC and KICH and higher tumor expression in HNSC, LUAD, COAD and STAD. The HNSC box plot shows higher CPZ RNA expression in tumor versus normal tissue (log2 FC = +1.073, t-test p < 0.001).
This table shows molecular features associated with CPZ in patient tissues and cancer cell lines. In patient samples, CPZ 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, CPZ RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BONE.
