Q-omics provides the consensus-scored BTG4 profile across patient tissues and cancer cell-line models. BTG4 expression is associated with patient survival in 17 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, BTG4 is differentially expressed in 7, with the highest sampling consensus in THCA. Additionally, BTG4 RNA expression shows 10,896 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight HNSC, THCA, and THYM as cancer lineages where BTG4 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 BTG4 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BTG4 survival associations across molecular data types. BTG4 RNA expression shows survival associations in the most cancer types (17), followed by mutation status (2) 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 BTG4 RNA expression–survival associations across cancer types. High BTG4 expression shows unfavorable associations in HNSC, KIRC, MESO and THCA, but favorable associations in LUSC and ESCA. The HNSC 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 HNSC as the clearest survival context for BTG4 RNA expression.
This table summarizes BTG4 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 4. The strongest signals are observed in THCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for BTG4. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BTG4 shows lower tumor expression in THCA and LUAD and higher tumor expression in HNSC, KIRC, BRCA and KIRP. The THCA box plot shows higher BTG4 RNA expression in normal versus tumor tissue (log2 FC = −0.096, t-test p < 0.001).
This table shows molecular features associated with BTG4 in patient tissues and cancer cell lines. In patient samples, BTG4 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, BTG4 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BONE.
