Q-omics provides the consensus-scored CPA1 profile across patient tissues and cancer cell-line models. CPA1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CPA1 is differentially expressed in 10, with the highest sampling consensus in KIRP. Additionally, CPA1 RNA expression shows 11,532 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRP, and TGCT as cancer lineages where CPA1 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 CPA1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CPA1 survival associations across molecular data types. CPA1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CPA1 RNA expression–survival associations across cancer types. High CPA1 expression shows unfavorable associations in KIRP, LGG, READ, BLCA and PAAD, but favorable associations in LUAD. The KIRP Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .003). Together, the overview and detailed table identify KIRP as the clearest survival context for CPA1 RNA expression.
This table summarizes CPA1 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 2. The strongest signals are observed in KIRP for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for CPA1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CPA1 shows lower tumor expression in KIRP, KIRC, LUAD, KICH, BRCA and UCEC. The KIRP box plot shows higher CPA1 RNA expression in normal versus tumor tissue (log2 FC = −0.649, t-test p < 0.001).
This table shows molecular features associated with CPA1 in patient tissues and cancer cell lines. In patient samples, CPA1 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, CPA1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in SKIN and LARGE_INTESTINE.
