Q-omics provides the consensus-scored CSNK1D profile across patient tissues and cancer cell-line models. CSNK1D expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, CSNK1D is differentially expressed in 12, with the highest sampling consensus in KIRP. Additionally, CSNK1D RNA expression shows 19,701 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight LIHC, KIRP, and ACC as cancer lineages where CSNK1D 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 CSNK1D — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CSNK1D survival associations across molecular data types. CSNK1D RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CSNK1D RNA expression–survival associations across cancer types. High CSNK1D expression shows unfavorable associations in LIHC, KICH, LUSC, HNSC and LGG, but favorable associations in BRCA. The LIHC 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 LIHC as the clearest survival context for CSNK1D RNA expression.
This table summarizes CSNK1D tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 4. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CSNK1D. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CSNK1D shows lower tumor expression in KICH and higher tumor expression in KIRP, HNSC, LIHC, STAD and CHOL. The KIRP box plot shows higher CSNK1D RNA expression in tumor versus normal tissue (log2 FC = +1.297, t-test p < 0.001).
This table shows molecular features associated with CSNK1D in patient tissues and cancer cell lines. In patient samples, CSNK1D 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, CSNK1D RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in CNS and UPPER_AERODIGESTIVE_TRACT.
