Q-omics provides the consensus-scored STK35 profile across patient tissues and cancer cell-line models. STK35 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, STK35 is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, STK35 RNA expression shows 20,172 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight COAD, HNSC, and KIRP as cancer lineages where STK35 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 STK35 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes STK35 survival associations across molecular data types. STK35 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (2) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible STK35 RNA expression–survival associations across cancer types. High STK35 expression shows unfavorable associations in COAD, LIHC, LGG, KIRP, KIRC and LUAD. The COAD 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 COAD as the clearest survival context for STK35 RNA expression.
This table summarizes STK35 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 STK35. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. STK35 shows higher tumor expression in HNSC, KIRC, KIRP, BLCA, COAD and LIHC. The HNSC box plot shows higher STK35 RNA expression in tumor versus normal tissue (log2 FC = +0.879, t-test p < 0.001).
This table shows molecular features associated with STK35 in patient tissues and cancer cell lines. In patient samples, STK35 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, STK35 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
