Q-omics provides the consensus-scored COBL profile across patient tissues and cancer cell-line models. COBL expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, COBL is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, COBL protein abundance shows 29,818 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, HNSC, and GBM as cancer lineages where COBL 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 COBL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes COBL survival associations across molecular data types. COBL RNA expression shows survival associations in the most cancer types (27), followed by mutation status (9) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible COBL RNA expression–survival associations across cancer types. High COBL expression shows unfavorable associations in UVM, BLCA, LUAD and HNSC, but favorable associations in KIRC and KIRP. 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 COBL RNA expression.
This table summarizes COBL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 12. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for COBL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. COBL shows lower tumor expression in HNSC, THCA, KIRC, LUSC, LUAD and COAD. The HNSC box plot shows higher COBL RNA expression in normal versus tumor tissue (log2 FC = −1.802, t-test p < 0.001).
This table shows molecular features associated with COBL in patient tissues and cancer cell lines. In patient samples, COBL 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, COBL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BREAST.
