Q-omics provides the consensus-scored BTBD3 profile across patient tissues and cancer cell-line models. BTBD3 expression is associated with patient survival in 30 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, BTBD3 is differentially expressed in 12, with the highest sampling consensus in COAD. Additionally, BTBD3 RNA expression shows 20,783 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, COAD, and UVM as cancer lineages where BTBD3 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 BTBD3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BTBD3 survival associations across molecular data types. BTBD3 RNA expression shows survival associations in the most cancer types (30), followed by mutation status (6) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible BTBD3 RNA expression–survival associations across cancer types. High BTBD3 expression shows unfavorable associations in LIHC, MESO and SARC, but favorable associations in KIRC, SCLC 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 BTBD3 RNA expression.
This table summarizes BTBD3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 2. The strongest signals are observed in COAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for BTBD3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BTBD3 shows lower tumor expression in COAD and KICH and higher tumor expression in LIHC, KIRC, CHOL and HNSC. The COAD box plot shows higher BTBD3 RNA expression in normal versus tumor tissue (log2 FC = −0.882, t-test p < 0.001).
This table shows molecular features associated with BTBD3 in patient tissues and cancer cell lines. In patient samples, BTBD3 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, BTBD3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BLOOD_Leukemia.
