Q-omics provides the consensus-scored KRT6A profile across patient tissues and cancer cell-line models. KRT6A expression is associated with patient survival in 17 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, KRT6A is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, KRT6A protein abundance shows 16,082 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight KIRC, COAD, and HNSC as cancer lineages where KRT6A 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 KRT6A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KRT6A survival associations across molecular data types. KRT6A RNA expression shows survival associations in the most cancer types (17), followed by mutation status (8) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KRT6A RNA expression–survival associations across cancer types. High KRT6A expression shows unfavorable associations in KIRC, LUAD, PAAD, SKCM and LIHC, but favorable associations in LUSC. The KIRC 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 KIRC as the clearest survival context for KRT6A RNA expression.
This table summarizes KRT6A 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 5. The strongest signals are observed in COAD for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for KRT6A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KRT6A shows higher tumor expression in COAD, LUSC, LUAD, BLCA, THCA and HNSC. The COAD box plot shows higher KRT6A RNA expression in tumor versus normal tissue (log2 FC = +2.160, t-test p < 0.001).
This table shows molecular features associated with KRT6A in patient tissues and cancer cell lines. In patient samples, KRT6A shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, KRT6A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in CNS and BLOOD_Lymphoma.
