Q-omics provides the consensus-scored SRPK3 profile across patient tissues and cancer cell-line models. SRPK3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, SRPK3 is differentially expressed in 11, with the highest sampling consensus in BLCA. Additionally, SRPK3 RNA expression shows 16,758 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, BLCA, and UVM as cancer lineages where SRPK3 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 SRPK3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SRPK3 survival associations across molecular data types. SRPK3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible SRPK3 RNA expression–survival associations across cancer types. High SRPK3 expression shows unfavorable associations in KIRC, BRCA, UVM and MESO, but favorable associations in LUAD and PAAD. 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 SRPK3 RNA expression.
This table summarizes SRPK3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 1. The strongest signals are observed in BLCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for SRPK3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SRPK3 shows lower tumor expression in BLCA and HNSC and higher tumor expression in LUAD, CHOL, LIHC and BRCA. The BLCA box plot shows higher SRPK3 RNA expression in normal versus tumor tissue (log2 FC = −2.197, t-test p < 0.001).
This table shows molecular features associated with SRPK3 in patient tissues and cancer cell lines. In patient samples, SRPK3 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, SRPK3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in OVARY and BLOOD_Leukemia.
