Q-omics provides the consensus-scored KRT16 profile across patient tissues and cancer cell-line models. KRT16 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, KRT16 is differentially expressed in 14, with the highest sampling consensus in LUAD. Additionally, KRT16 protein abundance shows 18,037 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight KIRC, LUAD, and HNSC as cancer lineages where KRT16 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 KRT16 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KRT16 survival associations across molecular data types. KRT16 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) 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 KRT16 RNA expression–survival associations across cancer types. High KRT16 expression shows unfavorable associations in KIRC, LUAD, MESO, PAAD, LIHC and KIRP. 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 KRT16 RNA expression.
This table summarizes KRT16 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 4. The strongest signals are observed in LUAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for KRT16. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KRT16 shows higher tumor expression in LUAD, COAD, LUSC, BLCA, HNSC and UCEC. The LUAD box plot shows higher KRT16 RNA expression in tumor versus normal tissue (log2 FC = +3.400, t-test p < 0.001).
This table shows molecular features associated with KRT16 in patient tissues and cancer cell lines. In patient samples, KRT16 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, KRT16 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and BREAST.
