Q-omics provides the consensus-scored CPN2 profile across patient tissues and cancer cell-line models. CPN2 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, CPN2 is differentially expressed in 12, with the highest sampling consensus in KIRP. Additionally, CPN2 protein abundance shows 22,316 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, KIRP, and LSCC as cancer lineages where CPN2 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 CPN2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CPN2 survival associations across molecular data types. CPN2 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (6) 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 CPN2 RNA expression–survival associations across cancer types. High CPN2 expression shows unfavorable associations in ACC, THCA, CHOL and LGG, but favorable associations in LIHC and READ. The ACC 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 ACC as the clearest survival context for CPN2 RNA expression.
This table summarizes CPN2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRP for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for CPN2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CPN2 shows lower tumor expression in KIRP, KICH, KIRC and CHOL and higher tumor expression in HNSC and BRCA. The KIRP box plot shows higher CPN2 RNA expression in normal versus tumor tissue (log2 FC = −3.835, t-test p < 0.001).
This table shows molecular features associated with CPN2 in patient tissues and cancer cell lines. In patient samples, CPN2 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, CPN2 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 SKIN and LARGE_INTESTINE.
