Q-omics provides the consensus-scored SRPX profile across patient tissues and cancer cell-line models. SRPX expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, SRPX is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, SRPX protein abundance shows 23,908 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRP, COAD, and LUAD as cancer lineages where SRPX 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 SRPX — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SRPX survival associations across molecular data types. SRPX RNA expression shows survival associations in the most cancer types (23), followed by mutation status (8) 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 SRPX RNA expression–survival associations across cancer types. High SRPX expression shows unfavorable associations in KIRP, HNSC, UCEC, BLCA, UVM and MESO. The KIRP 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 KIRP as the clearest survival context for SRPX RNA expression.
This table summarizes SRPX 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 7. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for SRPX. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SRPX shows lower tumor expression in COAD, BLCA, LUAD, THCA, UCEC and LIHC. The COAD box plot shows higher SRPX RNA expression in normal versus tumor tissue (log2 FC = −2.285, t-test p < 0.001).
This table shows molecular features associated with SRPX in patient tissues and cancer cell lines. In patient samples, SRPX 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, SRPX RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in OVARY and SOFT_TISSUE.
