Q-omics provides the consensus-scored STK32A profile across patient tissues and cancer cell-line models. STK32A expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, STK32A is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, STK32A RNA expression shows 17,020 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight ACC, KIRC, and UVM as cancer lineages where STK32A 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 STK32A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes STK32A survival associations across molecular data types. STK32A RNA expression shows survival associations in the most cancer types (22), followed by mutation status (5) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible STK32A RNA expression–survival associations across cancer types. High STK32A expression shows unfavorable associations in CESC, STAD and UVM, but favorable associations in ACC, LUAD and MESO. The ACC 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 ACC as the clearest survival context for STK32A RNA expression.
This table summarizes STK32A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for STK32A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. STK32A shows lower tumor expression in KIRC, COAD and KIRP and higher tumor expression in THCA, LUAD and BLCA. The KIRC box plot shows higher STK32A RNA expression in normal versus tumor tissue (log2 FC = −1.806, t-test p < 0.001).
This table shows molecular features associated with STK32A in patient tissues and cancer cell lines. In patient samples, STK32A shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, STK32A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and LUNG_SCLC.