Q-omics provides the consensus-scored BLVRB profile across patient tissues and cancer cell-line models. BLVRB expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in CHOL. Among the 18 cancer types available for tumor–normal comparison, BLVRB is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, BLVRB protein abundance shows 22,144 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight CHOL, KIRC, and LUAD as cancer lineages where BLVRB 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 BLVRB — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BLVRB survival associations across molecular data types. BLVRB RNA expression shows survival associations in the most cancer types (20), followed by mutation status (1) 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 BLVRB RNA expression–survival associations across cancer types. High BLVRB expression shows unfavorable associations in CHOL, LGG, PAAD, UCS, LUAD and GBM. The CHOL Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify CHOL as the clearest survival context for BLVRB RNA expression.
This table summarizes BLVRB tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 8. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for BLVRB. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BLVRB shows lower tumor expression in THCA, KICH and HNSC and higher tumor expression in KIRC, KIRP and LIHC. The KIRC box plot shows higher BLVRB RNA expression in tumor versus normal tissue (log2 FC = +0.910, t-test p < 0.001).
This table shows molecular features associated with BLVRB in patient tissues and cancer cell lines. In patient samples, BLVRB 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, BLVRB RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Leukemia.
