Q-omics provides the consensus-scored CAPN6 profile across patient tissues and cancer cell-line models. CAPN6 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in UCS. Among the 18 cancer types available for tumor–normal comparison, CAPN6 is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, CAPN6 protein abundance shows 25,556 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight UCS, HNSC, and GBM as cancer lineages where CAPN6 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 CAPN6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CAPN6 survival associations across molecular data types. CAPN6 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CAPN6 RNA expression–survival associations across cancer types. High CAPN6 expression shows unfavorable associations in LIHC, LAML, LGG and DLBC, but favorable associations in UCS and BRCA. The UCS Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .007). Together, the overview and detailed table identify UCS as the clearest survival context for CAPN6 RNA expression.
This table summarizes CAPN6 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 8. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CAPN6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CAPN6 shows lower tumor expression in HNSC, KICH, KIRC, THCA, BLCA and BRCA. The HNSC box plot shows higher CAPN6 RNA expression in normal versus tumor tissue (log2 FC = −2.062, t-test p < 0.001).
This table shows molecular features associated with CAPN6 in patient tissues and cancer cell lines. In patient samples, CAPN6 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, CAPN6 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 STOMACH and SOFT_TISSUE.
