Q-omics provides the consensus-scored CCIN profile across patient tissues and cancer cell-line models. CCIN expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, CCIN is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, CCIN RNA expression shows 13,752 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRP, HNSC, and THYM as cancer lineages where CCIN 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 CCIN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CCIN survival associations across molecular data types. CCIN RNA expression shows survival associations in the most cancer types (23), followed by mutation status (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CCIN RNA expression–survival associations across cancer types. High CCIN expression shows unfavorable associations in KIRP, BLCA, MESO, UCEC and THCA, but favorable associations in UCS. The KIRP 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 KIRP as the clearest survival context for CCIN RNA expression.
This table summarizes CCIN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for CCIN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CCIN shows lower tumor expression in BLCA, LUAD and LUSC and higher tumor expression in HNSC, BRCA and LIHC. The HNSC box plot shows higher CCIN RNA expression in tumor versus normal tissue (log2 FC = +0.269, t-test p < 0.001).
This table shows molecular features associated with CCIN in patient tissues and cancer cell lines. In patient samples, CCIN shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, CCIN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
