Q-omics provides the consensus-scored BNIP1 profile across patient tissues and cancer cell-line models. BNIP1 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, BNIP1 is differentially expressed in 13, with the highest sampling consensus in LIHC. Additionally, BNIP1 RNA expression shows 18,151 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight UVM, LIHC, and ACC as cancer lineages where BNIP1 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 BNIP1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BNIP1 survival associations across molecular data types. BNIP1 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (1) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible BNIP1 RNA expression–survival associations across cancer types. High BNIP1 expression shows unfavorable associations in UVM, KICH, ESCA, CESC, KIRP and HNSC. The UVM 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 UVM as the clearest survival context for BNIP1 RNA expression.
This table summarizes BNIP1 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 LIHC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for BNIP1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BNIP1 shows lower tumor expression in THCA and higher tumor expression in LIHC, HNSC, BLCA, STAD and BRCA. The LIHC box plot shows higher BNIP1 RNA expression in tumor versus normal tissue (log2 FC = +0.979, t-test p < 0.001).
This table shows molecular features associated with BNIP1 in patient tissues and cancer cell lines. In patient samples, BNIP1 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, BNIP1 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 BLOOD_Leukemia and UPPER_AERODIGESTIVE_TRACT.
