Q-omics provides the consensus-scored STK33 profile across patient tissues and cancer cell-line models. STK33 expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, STK33 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, STK33 RNA expression shows 17,978 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight LUAD, KIRC, and THYM as cancer lineages where STK33 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 STK33 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes STK33 survival associations across molecular data types. STK33 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible STK33 RNA expression–survival associations across cancer types. High STK33 expression shows unfavorable associations in UVM, LGG, STAD and BLCA, but favorable associations in LUAD and SKCM. The LUAD 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 LUAD as the clearest survival context for STK33 RNA expression.
This table summarizes STK33 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for STK33. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. STK33 shows lower tumor expression in KIRC, LUSC, THCA, BLCA, LUAD and KICH. The KIRC box plot shows higher STK33 RNA expression in normal versus tumor tissue (log2 FC = −1.555, t-test p < 0.001).
This table shows molecular features associated with STK33 in patient tissues and cancer cell lines. In patient samples, STK33 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, STK33 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 LARGE_INTESTINE and LUNG_SCLC.
