Q-omics provides the consensus-scored CSNK1A1L profile across patient tissues and cancer cell-line models. CSNK1A1L expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in STAD. Among the 18 cancer types available for tumor–normal comparison, CSNK1A1L is differentially expressed in 8, with the highest sampling consensus in THCA. Additionally, CSNK1A1L RNA expression shows 10,266 significant gene co-expression associations, with the highest sampling consensus in KICH. Together, these results highlight STAD, THCA, and KICH as cancer lineages where CSNK1A1L 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 CSNK1A1L — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CSNK1A1L survival associations across molecular data types. CSNK1A1L RNA expression shows survival associations in the most cancer types (18), followed by mutation status (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CSNK1A1L RNA expression–survival associations across cancer types. High CSNK1A1L expression shows unfavorable associations in STAD and BLCA, but favorable associations in LGG, LUSC, PAAD and GBM. The STAD 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 STAD as the clearest survival context for CSNK1A1L RNA expression.
This table summarizes CSNK1A1L tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8. The strongest signals are observed in THCA for RNA.
This table ranks reproducible tumor–normal expression differences for CSNK1A1L. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CSNK1A1L shows lower tumor expression in THCA, KICH, BRCA, LUSC and READ and higher tumor expression in COAD. The THCA box plot shows higher CSNK1A1L RNA expression in normal versus tumor tissue (log2 FC = −0.146, t-test p < 0.001).
This table shows molecular features associated with CSNK1A1L in patient tissues and cancer cell lines. In patient samples, CSNK1A1L shows the broadest associations at the RNA and protein expression levels, with KICH recurring as the lineage with the largest associated feature set. In cancer cell lines, CSNK1A1L 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 BONE and BLOOD_Leukemia.
