Q-omics provides the consensus-scored BTG3 profile across patient tissues and cancer cell-line models. BTG3 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, BTG3 is differentially expressed in 14, with the highest sampling consensus in LIHC. Additionally, BTG3 RNA expression shows 18,112 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, LIHC, and UVM as cancer lineages where BTG3 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 BTG3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BTG3 survival associations across molecular data types. BTG3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) 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 BTG3 RNA expression–survival associations across cancer types. High BTG3 expression shows unfavorable associations in KIRC, ACC, LIHC, LGG and UVM, but favorable associations in LUSC. 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 BTG3 RNA expression.
This table summarizes BTG3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 1. The strongest signals are observed in LIHC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for BTG3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BTG3 shows lower tumor expression in KIRC, KIRP and LUSC and higher tumor expression in LIHC, HNSC and CHOL. The LIHC box plot shows higher BTG3 RNA expression in tumor versus normal tissue (log2 FC = +1.520, t-test p < 0.001).
This table shows molecular features associated with BTG3 in patient tissues and cancer cell lines. In patient samples, BTG3 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, BTG3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in BREAST and LARGE_INTESTINE.
