Q-omics provides the consensus-scored BTG1 profile across patient tissues and cancer cell-line models. BTG1 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, BTG1 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, BTG1 RNA expression shows 18,503 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRP, KIRC, and ACC as cancer lineages where BTG1 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 BTG1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BTG1 survival associations across molecular data types. BTG1 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (2) 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 BTG1 RNA expression–survival associations across cancer types. High BTG1 expression shows unfavorable associations in KIRP and LUAD, but favorable associations in BRCA, UVM, HNSC and LUSC. The KIRP 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 KIRP as the clearest survival context for BTG1 RNA expression.
This table summarizes BTG1 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 2. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for BTG1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BTG1 shows lower tumor expression in COAD, UCEC, KICH and LUAD and higher tumor expression in KIRC and HNSC. The KIRC box plot shows higher BTG1 RNA expression in tumor versus normal tissue (log2 FC = +0.883, t-test p < 0.001).
This table shows molecular features associated with BTG1 in patient tissues and cancer cell lines. In patient samples, BTG1 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, BTG1 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 LUNG_NSCLC_LUAD and BLOOD_Leukemia.
