Q-omics provides the consensus-scored CUTC profile across patient tissues and cancer cell-line models. CUTC expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, CUTC is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, CUTC RNA expression shows 18,633 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KICH, KIRC, and UVM as cancer lineages where CUTC 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 CUTC — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CUTC survival associations across molecular data types. CUTC RNA expression shows survival associations in the most cancer types (21), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CUTC RNA expression–survival associations across cancer types. High CUTC expression shows unfavorable associations in KICH, ACC, KIRP and UVM, but favorable associations in SKCM and LGG. The KICH 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 KICH as the clearest survival context for CUTC RNA expression.
This table summarizes CUTC 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 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CUTC. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CUTC shows lower tumor expression in BLCA, KICH and BRCA and higher tumor expression in KIRC, LIHC and CHOL. The KIRC box plot shows higher CUTC RNA expression in tumor versus normal tissue (log2 FC = +0.586, t-test p < 0.001).
This table shows molecular features associated with CUTC in patient tissues and cancer cell lines. In patient samples, CUTC shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, CUTC RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in BONE and BLOOD_Lymphoma.
