Q-omics provides the consensus-scored CMPK1 profile across patient tissues and cancer cell-line models. CMPK1 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CMPK1 is differentially expressed in 13, with the highest sampling consensus in THCA. Additionally, CMPK1 RNA expression shows 19,617 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRP, THCA, and ACC as cancer lineages where CMPK1 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 CMPK1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CMPK1 survival associations across molecular data types. CMPK1 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (3) 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 CMPK1 RNA expression–survival associations across cancer types. High CMPK1 expression shows unfavorable associations in KIRP, ACC, MESO, ESCA, LGG and KICH. 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 CMPK1 RNA expression.
This table summarizes CMPK1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 7. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CMPK1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CMPK1 shows lower tumor expression in THCA, KICH and HNSC and higher tumor expression in KIRC, STAD and LUAD. The THCA box plot shows higher CMPK1 RNA expression in normal versus tumor tissue (log2 FC = −0.536, t-test p < 0.001).
This table shows molecular features associated with CMPK1 in patient tissues and cancer cell lines. In patient samples, CMPK1 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, CMPK1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BONE.
