Q-omics provides the consensus-scored CMPK2 profile across patient tissues and cancer cell-line models. CMPK2 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, CMPK2 is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, CMPK2 RNA expression shows 16,863 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight SKCM, HNSC, and THYM as cancer lineages where CMPK2 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 CMPK2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CMPK2 survival associations across molecular data types. CMPK2 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CMPK2 RNA expression–survival associations across cancer types. High CMPK2 expression shows unfavorable associations in UVM, UCEC, KICH and LGG, but favorable associations in SKCM and KIRC. The SKCM 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 SKCM as the clearest survival context for CMPK2 RNA expression.
This table summarizes CMPK2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CMPK2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CMPK2 shows lower tumor expression in KICH and higher tumor expression in HNSC, KIRC, BLCA, STAD and BRCA. The HNSC box plot shows higher CMPK2 RNA expression in tumor versus normal tissue (log2 FC = +2.386, t-test p < 0.001).
This table shows molecular features associated with CMPK2 in patient tissues and cancer cell lines. In patient samples, CMPK2 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, CMPK2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUSC and BLOOD_Leukemia.
