Q-omics provides the consensus-scored KRTAP10-11 profile across patient tissues and cancer cell-line models. KRTAP10-11 expression is associated with patient survival in 11 of 34 cancer types, with the highest sampling consensus in UCEC. Among the 18 cancer types available for tumor–normal comparison, KRTAP10-11 is differentially expressed in 1, with the highest sampling consensus in HNSC. Additionally, KRTAP10-11 RNA expression shows 6,310 significant pathway-activity associations, with the highest sampling consensus in STAD. Together, these results highlight UCEC, HNSC, and STAD as cancer lineages where KRTAP10-11 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 KRTAP10-11 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KRTAP10-11 survival associations across molecular data types. KRTAP10-11 RNA expression shows survival associations in the most cancer types (11), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KRTAP10-11 RNA expression–survival associations across cancer types. High KRTAP10-11 expression shows unfavorable associations in UCEC, SKCM, OV, BLCA, ACC and LGG. The UCEC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .015). Together, the overview and detailed table identify UCEC as the clearest survival context for KRTAP10-11 RNA expression.
This table summarizes KRTAP10-11 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 1. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for KRTAP10-11. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KRTAP10-11 shows higher tumor expression in HNSC. The HNSC box plot shows higher KRTAP10-11 RNA expression in tumor versus normal tissue (log2 FC = +0.012, t-test p = .029).
This table shows molecular features associated with KRTAP10-11 in patient tissues and cancer cell lines. In patient samples, KRTAP10-11 shows the broadest associations at the RNA and protein expression levels, with STAD recurring as the lineage with the largest associated feature set. In cancer cell lines, KRTAP10-11 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in CNS and BONE.
