Q-omics provides the consensus-scored KRT3 profile across patient tissues and cancer cell-line models. KRT3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, KRT3 is differentially expressed in 9, with the highest sampling consensus in HNSC. Additionally, KRT3 RNA expression shows 10,084 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, HNSC, and TGCT as cancer lineages where KRT3 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 KRT3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KRT3 survival associations across molecular data types. KRT3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KRT3 RNA expression–survival associations across cancer types. High KRT3 expression shows unfavorable associations in KIRC, COAD, BRCA, STAD, LIHC and BLCA. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .007). Together, the overview and detailed table identify KIRC as the clearest survival context for KRT3 RNA expression.
This table summarizes KRT3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 3. The strongest signals are observed in HNSC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for KRT3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KRT3 shows lower tumor expression in HNSC and higher tumor expression in LUSC, BRCA, LUAD, BLCA and KIRP. The HNSC box plot shows higher KRT3 RNA expression in normal versus tumor tissue (log2 FC = −2.264, t-test p < 0.001).
This table shows molecular features associated with KRT3 in patient tissues and cancer cell lines. In patient samples, KRT3 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, KRT3 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 LUNG_SCLC and LUNG_NSCLC_LUAD.
