Q-omics provides the consensus-scored BTBD9 profile across patient tissues and cancer cell-line models. BTBD9 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, BTBD9 is differentially expressed in 15, with the highest sampling consensus in LIHC. Additionally, BTBD9 RNA expression shows 20,991 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, LIHC, and ACC as cancer lineages where BTBD9 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 BTBD9 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BTBD9 survival associations across molecular data types. BTBD9 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (7) 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 BTBD9 RNA expression–survival associations across cancer types. High BTBD9 expression shows unfavorable associations in DLBC, but favorable associations in KIRC, LUAD, KIRP, HNSC and READ. 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 BTBD9 RNA expression.
This table summarizes BTBD9 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 4. The strongest signals are observed in LIHC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for BTBD9. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BTBD9 shows lower tumor expression in COAD, LUSC, LUAD and KIRC and higher tumor expression in LIHC and BRCA. The LIHC box plot shows higher BTBD9 RNA expression in tumor versus normal tissue (log2 FC = +1.014, t-test p < 0.001).
This table shows molecular features associated with BTBD9 in patient tissues and cancer cell lines. In patient samples, BTBD9 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, BTBD9 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 BONE and LARGE_INTESTINE.
