Q-omics provides the consensus-scored BUD23 profile across patient tissues and cancer cell-line models. BUD23 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, BUD23 is differentially expressed in 17, with the highest sampling consensus in COAD. Additionally, BUD23 protein abundance shows 22,198 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, COAD, and GBM as cancer lineages where BUD23 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 BUD23 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BUD23 survival associations across molecular data types. BUD23 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) 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 BUD23 RNA expression–survival associations across cancer types. High BUD23 expression shows unfavorable associations in KIRC, UVM, KICH, ACC, LUAD and LGG. The KIRC 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 KIRC as the clearest survival context for BUD23 RNA expression.
This table summarizes BUD23 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 5. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for BUD23. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BUD23 shows higher tumor expression in COAD, STAD, LIHC, LUAD, KIRP and HNSC. The COAD box plot shows higher BUD23 RNA expression in tumor versus normal tissue (log2 FC = +1.171, t-test p < 0.001).
This table shows molecular features associated with BUD23 in patient tissues and cancer cell lines. In patient samples, BUD23 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, BUD23 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and UPPER_AERODIGESTIVE_TRACT.
