Q-omics provides the consensus-scored CPT1A profile across patient tissues and cancer cell-line models. CPT1A expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CPT1A is differentially expressed in 10, with the highest sampling consensus in COAD. Additionally, CPT1A protein abundance shows 19,787 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRC, COAD, and PDAC as cancer lineages where CPT1A 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 CPT1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CPT1A survival associations across molecular data types. CPT1A RNA expression shows survival associations in the most cancer types (25), followed by mutation status (9) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CPT1A RNA expression–survival associations across cancer types. High CPT1A expression shows unfavorable associations in ACC, OV, CHOL and BRCA, but favorable associations in KIRC and SKCM. The KIRC 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 KIRC as the clearest survival context for CPT1A RNA expression.
This table summarizes CPT1A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 9. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CPT1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CPT1A shows lower tumor expression in COAD, KIRP, THCA and KIRC and higher tumor expression in STAD and HNSC. The COAD box plot shows higher CPT1A RNA expression in normal versus tumor tissue (log2 FC = −1.189, t-test p < 0.001).
This table shows molecular features associated with CPT1A in patient tissues and cancer cell lines. In patient samples, CPT1A shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, CPT1A 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 SOFT_TISSUE and BREAST.
