Q-omics provides the consensus-scored STK26 profile across patient tissues and cancer cell-line models. STK26 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, STK26 is differentially expressed in 15, with the highest sampling consensus in LUAD. Additionally, STK26 protein abundance shows 20,054 significant protein co-abundance associations, with the highest sampling consensus in UCEC. Together, these results highlight KIRP, LUAD, and UCEC as cancer lineages where STK26 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 STK26 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes STK26 survival associations across molecular data types. STK26 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (6) 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 STK26 RNA expression–survival associations across cancer types. High STK26 expression shows unfavorable associations in KIRP, LIHC, UVM and LUAD, but favorable associations in LAML and UCS. The KIRP Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .002). Together, the overview and detailed table identify KIRP as the clearest survival context for STK26 RNA expression.
This table summarizes STK26 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for STK26. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. STK26 shows lower tumor expression in KIRC and higher tumor expression in LUAD, HNSC, STAD, LUSC and BRCA. The LUAD box plot shows higher STK26 RNA expression in tumor versus normal tissue (log2 FC = +1.012, t-test p < 0.001).
This table shows molecular features associated with STK26 in patient tissues and cancer cell lines. In patient samples, STK26 shows the broadest associations at the RNA and protein expression levels, with UCEC recurring as the lineage with the largest associated feature set. In cancer cell lines, STK26 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and SOFT_TISSUE.
