Q-omics provides the consensus-scored KRTAP3-3 profile across patient tissues and cancer cell-line models. KRTAP3-3 expression is associated with patient survival in 13 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, KRTAP3-3 is differentially expressed in 4, with the highest sampling consensus in HNSC. Additionally, KRTAP3-3 RNA expression shows 5,142 significant pathway-activity associations, with the highest sampling consensus in STAD. Together, these results highlight ACC, HNSC, and STAD as cancer lineages where KRTAP3-3 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 KRTAP3-3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KRTAP3-3 survival associations across molecular data types. KRTAP3-3 RNA expression shows survival associations in the most cancer types (13), followed by mutation status (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KRTAP3-3 RNA expression–survival associations across cancer types. High KRTAP3-3 expression shows unfavorable associations in ACC, LIHC, SKCM, BLCA and STAD, but favorable associations in UCS. The ACC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify ACC as the clearest survival context for KRTAP3-3 RNA expression.
This table summarizes KRTAP3-3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 4. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for KRTAP3-3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KRTAP3-3 shows lower tumor expression in HNSC and PRAD and higher tumor expression in LUSC and COAD. The HNSC box plot shows higher KRTAP3-3 RNA expression in normal versus tumor tissue (log2 FC = −0.891, t-test p = .005).
This table shows molecular features associated with KRTAP3-3 in patient tissues and cancer cell lines. In patient samples, KRTAP3-3 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, KRTAP3-3 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 URINARY_TRACT and LARGE_INTESTINE.
