Q-omics provides the consensus-scored SRPRB profile across patient tissues and cancer cell-line models. SRPRB expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, SRPRB is differentially expressed in 17, with the highest sampling consensus in THCA. Additionally, SRPRB protein abundance shows 18,929 significant protein co-abundance associations, with the highest sampling consensus in CCRCC. Together, these results highlight MESO, THCA, and CCRCC as cancer lineages where SRPRB 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 SRPRB — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes SRPRB survival associations across molecular data types. SRPRB RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3) 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 SRPRB RNA expression–survival associations across cancer types. High SRPRB expression shows unfavorable associations in MESO, KICH, ACC, BLCA, LIHC and HNSC. 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 SRPRB RNA expression.
This table summarizes SRPRB 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 THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for SRPRB. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. SRPRB shows lower tumor expression in THCA and higher tumor expression in LIHC, COAD, LUAD, KIRP and LUSC. The THCA box plot shows higher SRPRB RNA expression in normal versus tumor tissue (log2 FC = −1.412, t-test p < 0.001).
This table shows molecular features associated with SRPRB in patient tissues and cancer cell lines. In patient samples, SRPRB shows the broadest associations at the RNA and protein expression levels, with CCRCC recurring as the lineage with the largest associated feature set. In cancer cell lines, SRPRB RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Lymphoma.
