Q-omics provides the consensus-scored BTN3A2 profile across patient tissues and cancer cell-line models. BTN3A2 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, BTN3A2 is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, BTN3A2 RNA expression shows 16,692 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight SKCM, KIRC, and UVM as cancer lineages where BTN3A2 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 BTN3A2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BTN3A2 survival associations across molecular data types. BTN3A2 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (3) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible BTN3A2 RNA expression–survival associations across cancer types. High BTN3A2 expression shows unfavorable associations in LGG, but favorable associations in SKCM, READ, BLCA, MESO and OV. The SKCM 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 SKCM as the clearest survival context for BTN3A2 RNA expression.
This table summarizes BTN3A2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for BTN3A2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BTN3A2 shows lower tumor expression in LUSC and LUAD and higher tumor expression in KIRC, KIRP, HNSC and STAD. The KIRC box plot shows higher BTN3A2 RNA expression in tumor versus normal tissue (log2 FC = +2.091, t-test p < 0.001).
This table shows molecular features associated with BTN3A2 in patient tissues and cancer cell lines. In patient samples, BTN3A2 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, BTN3A2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Leukemia.
