Q-omics provides the consensus-scored CAPN2 profile across patient tissues and cancer cell-line models. CAPN2 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, CAPN2 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, CAPN2 protein abundance shows 31,783 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight BLCA, KIRC, and PDAC as cancer lineages where CAPN2 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 CAPN2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CAPN2 survival associations across molecular data types. CAPN2 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (6) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CAPN2 RNA expression–survival associations across cancer types. High CAPN2 expression shows unfavorable associations in BLCA, PAAD, LGG, ACC, UVM and BRCA. The BLCA Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .004). Together, the overview and detailed table identify BLCA as the clearest survival context for CAPN2 RNA expression.
This table summarizes CAPN2 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 6. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for CAPN2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CAPN2 shows lower tumor expression in KIRC, COAD, UCEC, LUSC and READ and higher tumor expression in LIHC. The KIRC box plot shows higher CAPN2 RNA expression in normal versus tumor tissue (log2 FC = −0.647, t-test p < 0.001).
This table shows molecular features associated with CAPN2 in patient tissues and cancer cell lines. In patient samples, CAPN2 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, CAPN2 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 CNS and BLOOD_Lymphoma.
