Q-omics provides the consensus-scored BSPRY profile across patient tissues and cancer cell-line models. BSPRY expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, BSPRY is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, BSPRY protein abundance shows 24,667 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight KIRC, and HNSC as cancer lineages where BSPRY 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 BSPRY — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BSPRY survival associations across molecular data types. BSPRY RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3) and mass-spec protein abundance (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible BSPRY RNA expression–survival associations across cancer types. High BSPRY expression shows unfavorable associations in LUSC, but favorable associations in KIRC, HNSC, LUAD, KIRP and LGG. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for BSPRY RNA expression.
This table summarizes BSPRY tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 10. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for BSPRY. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BSPRY shows lower tumor expression in KIRC, KIRP, HNSC and THCA and higher tumor expression in COAD and LUAD. The KIRC box plot shows higher BSPRY RNA expression in normal versus tumor tissue (log2 FC = −3.091, t-test p < 0.001).
This table shows molecular features associated with BSPRY in patient tissues and cancer cell lines. In patient samples, BSPRY shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, BSPRY RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in SKIN and LUNG_SCLC.
