Q-omics provides the consensus-scored BLVRA profile across patient tissues and cancer cell-line models. BLVRA expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, BLVRA is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, BLVRA protein abundance shows 22,747 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, and GBM as cancer lineages where BLVRA 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 BLVRA — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BLVRA survival associations across molecular data types. BLVRA RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible BLVRA RNA expression–survival associations across cancer types. High BLVRA expression shows unfavorable associations in LIHC, but favorable associations in KIRC, MESO, LUSC, BRCA and THCA. 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 BLVRA RNA expression.
This table summarizes BLVRA tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, 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 BLVRA. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BLVRA shows lower tumor expression in KICH and higher tumor expression in KIRC, KIRP, LIHC, THCA and BRCA. The KIRC box plot shows higher BLVRA RNA expression in tumor versus normal tissue (log2 FC = +0.877, t-test p < 0.001).
This table shows molecular features associated with BLVRA in patient tissues and cancer cell lines. In patient samples, BLVRA shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, BLVRA RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and CNS.
