Q-omics provides the consensus-scored RBAK profile across patient tissues and cancer cell-line models. RBAK expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, RBAK is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, RBAK RNA expression shows 21,346 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KICH, HNSC, and ACC as cancer lineages where RBAK 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 RBAK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes RBAK survival associations across molecular data types. RBAK RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible RBAK RNA expression–survival associations across cancer types. High RBAK expression shows unfavorable associations in KICH, CESC, LGG, MESO and UVM, but favorable associations in KIRC. The KICH 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 KICH as the clearest survival context for RBAK RNA expression.
This table summarizes RBAK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 3. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for RBAK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. RBAK shows lower tumor expression in THCA and higher tumor expression in HNSC, KIRP, BLCA, KIRC and COAD. The HNSC box plot shows higher RBAK RNA expression in tumor versus normal tissue (log2 FC = +0.824, t-test p < 0.001).
This table shows molecular features associated with RBAK in patient tissues and cancer cell lines. In patient samples, RBAK shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, RBAK RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Lymphoma.
