basal cell adhesion molecule (Lutheran blood group)Genealiases: AU · B-CAM · CD239 · F8/G253 · LU · MSK19
Q-omics provides the consensus-scored BCAM profile across patient tissues and cancer cell-line models. BCAM expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, BCAM is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, BCAM protein abundance shows 20,234 significant protein co-abundance associations, with the highest sampling consensus in CCRCC. Together, these results highlight KIRC, and CCRCC as cancer lineages where BCAM 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 BCAM — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes BCAM survival associations across molecular data types. BCAM RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5) 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 BCAM RNA expression–survival associations across cancer types. High BCAM expression shows unfavorable associations in ACC, COAD and UCEC, but favorable associations in KIRC, BLCA and LUAD. The KIRC 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 KIRC as the clearest survival context for BCAM RNA expression.
This table summarizes BCAM 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 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for BCAM. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. BCAM shows lower tumor expression in KIRC, KICH, THCA, LUSC and KIRP and higher tumor expression in HNSC. The KIRC box plot shows higher BCAM RNA expression in normal versus tumor tissue (log2 FC = −2.052, t-test p < 0.001).
This table shows molecular features associated with BCAM in patient tissues and cancer cell lines. In patient samples, BCAM shows the broadest associations at the RNA and protein expression levels, with CCRCC recurring as the lineage with the largest associated feature set. In cancer cell lines, BCAM RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUSC, while CRISPR and shRNA rows add functional-dependency signals in LIVER and LARGE_INTESTINE.
