Q-omics provides the consensus-scored BCAN profile across patient tissues and cancer cell-line models. BCAN expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, BCAN is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, BCAN RNA expression shows 16,116 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight LUAD, KIRC, and ACC as cancer lineages where BCAN 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 BCAN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BCAN survival associations across molecular data types. BCAN RNA expression shows survival associations in the most cancer types (23), followed by mutation status (11). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible BCAN RNA expression–survival associations across cancer types. High BCAN expression shows unfavorable associations in LUAD, MESO, LAML and SKCM, but favorable associations in LGG and GBM. The LUAD 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 LUAD as the clearest survival context for BCAN RNA expression.
This table summarizes BCAN 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 KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for BCAN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BCAN shows higher tumor expression in KIRC, KIRP, LUAD, LIHC, COAD and LUSC. The KIRC box plot shows higher BCAN RNA expression in tumor versus normal tissue (log2 FC = +1.227, t-test p < 0.001).
This table shows molecular features associated with BCAN in patient tissues and cancer cell lines. In patient samples, BCAN 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, BCAN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and SKIN.
