Q-omics provides the consensus-scored KRT33A profile across patient tissues and cancer cell-line models. KRT33A expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in CESC. Among the 18 cancer types available for tumor–normal comparison, KRT33A is differentially expressed in 9, with the highest sampling consensus in HNSC. Additionally, KRT33A protein abundance shows 18,901 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight CESC, HNSC, and LSCC as cancer lineages where KRT33A 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 KRT33A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KRT33A survival associations across molecular data types. KRT33A RNA expression shows survival associations in the most cancer types (18), followed by mutation status (8) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KRT33A RNA expression–survival associations across cancer types. High KRT33A expression shows unfavorable associations in MESO and LIHC, but favorable associations in CESC, STAD, LGG and PAAD. The CESC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify CESC as the clearest survival context for KRT33A RNA expression.
This table summarizes KRT33A 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 5. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for KRT33A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KRT33A shows lower tumor expression in HNSC and higher tumor expression in LUSC, BLCA, UCEC, KIRC and KIRP. The HNSC box plot shows higher KRT33A RNA expression in normal versus tumor tissue (log2 FC = −1.391, t-test p < 0.001).
This table shows molecular features associated with KRT33A in patient tissues and cancer cell lines. In patient samples, KRT33A shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, KRT33A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and LARGE_INTESTINE.
