Q-omics provides the consensus-scored CENPK profile across patient tissues and cancer cell-line models. CENPK expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, CENPK is differentially expressed in 15, with the highest sampling consensus in BLCA. Additionally, CENPK RNA expression shows 21,164 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight MESO, BLCA, and GBM as cancer lineages where CENPK 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 CENPK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CENPK survival associations across molecular data types. CENPK RNA expression shows survival associations in the most cancer types (25), followed by mutation status (2) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CENPK RNA expression–survival associations across cancer types. High CENPK expression shows unfavorable associations in MESO, KIRP, ACC, KICH, LIHC and KIRC. The MESO 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 MESO as the clearest survival context for CENPK RNA expression.
This table summarizes CENPK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 4. The strongest signals are observed in THCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for CENPK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CENPK shows higher tumor expression in BLCA, LUAD, KIRP, HNSC, KIRC and THCA. The BLCA box plot shows higher CENPK RNA expression in tumor versus normal tissue (log2 FC = +2.432, t-test p < 0.001).
This table shows molecular features associated with CENPK in patient tissues and cancer cell lines. In patient samples, CENPK shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, CENPK 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 PANCREAS and BLOOD_Leukemia.
