Q-omics provides the consensus-scored CRBN profile across patient tissues and cancer cell-line models. CRBN expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CRBN is differentially expressed in 11, with the highest sampling consensus in LUAD. Additionally, CRBN protein abundance shows 24,003 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, LUAD, and GBM as cancer lineages where CRBN 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 CRBN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CRBN survival associations across molecular data types. CRBN RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CRBN RNA expression–survival associations across cancer types. High CRBN expression shows unfavorable associations in SCLC and KICH, but favorable associations in KIRC, SKCM, LUAD and UCS. 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 CRBN RNA expression.
This table summarizes CRBN 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 9. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CRBN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CRBN shows lower tumor expression in LUAD, THCA, LUSC, HNSC, UCEC and BRCA. The LUAD box plot shows higher CRBN RNA expression in normal versus tumor tissue (log2 FC = −1.347, t-test p < 0.001).
This table shows molecular features associated with CRBN in patient tissues and cancer cell lines. In patient samples, CRBN 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, CRBN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BREAST.
