Q-omics provides the consensus-scored SRPK1 profile across patient tissues and cancer cell-line models. SRPK1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, SRPK1 is differentially expressed in 17, with the highest sampling consensus in LUAD. Additionally, SRPK1 protein abundance shows 26,590 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight MESO, and LUAD as cancer lineages where SRPK1 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 SRPK1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SRPK1 survival associations across molecular data types. SRPK1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) 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 SRPK1 RNA expression–survival associations across cancer types. High SRPK1 expression shows unfavorable associations in MESO, ACC, LIHC, SARC and KIRP, but favorable associations in READ. The MESO 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 MESO as the clearest survival context for SRPK1 RNA expression.
This table summarizes SRPK1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 7. The strongest signals are observed in LUAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for SRPK1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SRPK1 shows higher tumor expression in LUAD, LIHC, COAD, LUSC, STAD and BRCA. The LUAD box plot shows higher SRPK1 RNA expression in tumor versus normal tissue (log2 FC = +1.751, t-test p < 0.001).
This table shows molecular features associated with SRPK1 in patient tissues and cancer cell lines. In patient samples, SRPK1 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, SRPK1 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 UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
