Q-omics provides the consensus-scored CACNA1A profile across patient tissues and cancer cell-line models. CACNA1A expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in PAAD. Among the 18 cancer types available for tumor–normal comparison, CACNA1A is differentially expressed in 10, with the highest sampling consensus in COAD. Additionally, CACNA1A RNA expression shows 12,689 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight PAAD, COAD, and TGCT as cancer lineages where CACNA1A 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 CACNA1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CACNA1A survival associations across molecular data types. CACNA1A RNA expression shows survival associations in the most cancer types (24), followed by mutation status (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CACNA1A RNA expression–survival associations across cancer types. High CACNA1A expression shows unfavorable associations in MESO and KIRC, but favorable associations in PAAD, LGG, HNSC and ACC. The PAAD 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 PAAD as the clearest survival context for CACNA1A RNA expression.
This table summarizes CACNA1A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10. The strongest signals are observed in COAD for RNA.
This table ranks reproducible tumor–normal expression differences for CACNA1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CACNA1A shows lower tumor expression in COAD and READ and higher tumor expression in HNSC, LUSC, KIRC and LIHC. The COAD box plot shows higher CACNA1A RNA expression in normal versus tumor tissue (log2 FC = −0.292, t-test p < 0.001).
This table shows molecular features associated with CACNA1A in patient tissues and cancer cell lines. In patient samples, CACNA1A shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, CACNA1A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUSC and LUNG_SCLC.