Q-omics provides the consensus-scored KRT76 profile across patient tissues and cancer cell-line models. KRT76 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, KRT76 is differentially expressed in 5, with the highest sampling consensus in HNSC. Additionally, KRT76 protein abundance shows 7,522 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight LUAD, HNSC, and PDAC as cancer lineages where KRT76 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 KRT76 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KRT76 survival associations across molecular data types. KRT76 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (7) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KRT76 RNA expression–survival associations across cancer types. High KRT76 expression shows unfavorable associations in LUAD, SKCM, GBM and KICH, but favorable associations in SCLC and LUSC. The LUAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify LUAD as the clearest survival context for KRT76 RNA expression.
This table summarizes KRT76 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 5, while mass-spec protein shows differences in 4. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for KRT76. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KRT76 shows lower tumor expression in HNSC, STAD and KIRP and higher tumor expression in LUSC and BLCA. The HNSC box plot shows higher KRT76 RNA expression in normal versus tumor tissue (log2 FC = −2.083, t-test p < 0.001).
This table shows molecular features associated with KRT76 in patient tissues and cancer cell lines. In patient samples, KRT76 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, KRT76 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Leukemia, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LUNG_NSCLC_LUAD.
