Q-omics provides the consensus-scored KPTN profile across patient tissues and cancer cell-line models. KPTN expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, KPTN is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, KPTN RNA expression shows 19,156 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, HNSC, and ACC as cancer lineages where KPTN 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 KPTN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes KPTN survival associations across molecular data types. KPTN RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible KPTN RNA expression–survival associations across cancer types. High KPTN expression shows unfavorable associations in KIRC, UVM, ACC, LIHC, COAD and LUAD. The KIRC 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 KIRC as the clearest survival context for KPTN RNA expression.
This table summarizes KPTN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 4. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for KPTN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. KPTN shows lower tumor expression in KICH and THCA and higher tumor expression in HNSC, LIHC, BLCA and STAD. The HNSC box plot shows higher KPTN RNA expression in tumor versus normal tissue (log2 FC = +0.607, t-test p < 0.001).
This table shows molecular features associated with KPTN in patient tissues and cancer cell lines. In patient samples, KPTN shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, KPTN 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 LUNG_NSCLC_LUAD and LARGE_INTESTINE.
