Q-omics provides the consensus-scored CACNA1F profile across patient tissues and cancer cell-line models. CACNA1F expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in BRCA. Among the 18 cancer types available for tumor–normal comparison, CACNA1F is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, CACNA1F RNA expression shows 15,306 significant gene co-expression associations, with the highest sampling consensus in LIHC. Together, these results highlight BRCA, KIRC, and LIHC as cancer lineages where CACNA1F 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 CACNA1F — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CACNA1F survival associations across molecular data types. CACNA1F RNA expression shows survival associations in the most cancer types (22), followed by mutation status (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CACNA1F RNA expression–survival associations across cancer types. High CACNA1F expression shows unfavorable associations in LUSC, LIHC and COAD, but favorable associations in BRCA, HNSC and BLCA. The BRCA Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify BRCA as the clearest survival context for CACNA1F RNA expression.
This table summarizes CACNA1F 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 1. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CACNA1F. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CACNA1F shows lower tumor expression in KICH, LUAD and LUSC and higher tumor expression in KIRC, HNSC and STAD. The KIRC box plot shows higher CACNA1F RNA expression in tumor versus normal tissue (log2 FC = +0.490, t-test p < 0.001).
This table shows molecular features associated with CACNA1F in patient tissues and cancer cell lines. In patient samples, CACNA1F shows the broadest associations at the RNA and protein expression levels, with LIHC recurring as the lineage with the largest associated feature set. In cancer cell lines, CACNA1F RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Leukemia.
