Q-omics provides the consensus-scored CBARP profile across patient tissues and cancer cell-line models. CBARP expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, CBARP is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, CBARP protein abundance shows 18,485 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, KIRC, and GBM as cancer lineages where CBARP 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 CBARP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CBARP survival associations across molecular data types. CBARP RNA expression shows survival associations in the most cancer types (23), followed by mutation status (3) 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 CBARP RNA expression–survival associations across cancer types. High CBARP expression shows unfavorable associations in ACC, BLCA, MESO, UVM, KICH and LIHC. The ACC 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 ACC as the clearest survival context for CBARP RNA expression.
This table summarizes CBARP 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 3. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CBARP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CBARP shows lower tumor expression in KIRC and KIRP and higher tumor expression in COAD, LUAD, HNSC and THCA. The KIRC box plot shows higher CBARP RNA expression in normal versus tumor tissue (log2 FC = −1.183, t-test p < 0.001).
This table shows molecular features associated with CBARP in patient tissues and cancer cell lines. In patient samples, CBARP shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, CBARP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and LARGE_INTESTINE.
