Q-omics provides the consensus-scored CRB3 profile across patient tissues and cancer cell-line models. CRB3 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, CRB3 is differentially expressed in 12, with the highest sampling consensus in BLCA. Additionally, CRB3 RNA expression shows 18,132 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRC, BLCA, and KIRP as cancer lineages where CRB3 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 CRB3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CRB3 survival associations across molecular data types. CRB3 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (2) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CRB3 RNA expression–survival associations across cancer types. High CRB3 expression shows unfavorable associations in CHOL, but favorable associations in KIRC, BLCA, UVM, UCEC and HNSC. 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 CRB3 RNA expression.
This table summarizes CRB3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 4. The strongest signals are observed in BLCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for CRB3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CRB3 shows higher tumor expression in BLCA, UCEC, BRCA, LIHC, THCA and CHOL. The BLCA box plot shows higher CRB3 RNA expression in tumor versus normal tissue (log2 FC = +2.272, t-test p = .023).
This table shows molecular features associated with CRB3 in patient tissues and cancer cell lines. In patient samples, CRB3 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, CRB3 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 LUNG_NSCLC_LUSC and LUNG_NSCLC_LUAD.
