Q-omics provides the consensus-scored KRT33B profile across patient tissues and cancer cell-line models. KRT33B expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, KRT33B is differentially expressed in 7, with the highest sampling consensus in KIRP. Additionally, KRT33B protein abundance shows 22,743 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRP, and LUAD as cancer lineages where KRT33B 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 KRT33B — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KRT33B survival associations across molecular data types. KRT33B RNA expression shows survival associations in the most cancer types (21), followed by mutation status (6) 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 KRT33B RNA expression–survival associations across cancer types. High KRT33B expression shows unfavorable associations in THCA, MESO, OV and DLBC, but favorable associations in KIRP and ESCA. The KIRP Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify KIRP as the clearest survival context for KRT33B RNA expression.
This table summarizes KRT33B tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRP for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for KRT33B. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KRT33B shows lower tumor expression in HNSC and higher tumor expression in KIRP, PAAD, BLCA, LUSC and KIRC. The KIRP box plot shows higher KRT33B RNA expression in tumor versus normal tissue (log2 FC = +0.251, t-test p < 0.001).
This table shows molecular features associated with KRT33B in patient tissues and cancer cell lines. In patient samples, KRT33B shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, KRT33B RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BONE.
