Q-omics provides the consensus-scored CTIF profile across patient tissues and cancer cell-line models. CTIF expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, CTIF is differentially expressed in 14, with the highest sampling consensus in LUAD. Additionally, CTIF protein abundance shows 32,536 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight BLCA, LUAD, and PDAC as cancer lineages where CTIF 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 CTIF — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CTIF survival associations across molecular data types. CTIF RNA expression shows survival associations in the most cancer types (27), followed by mutation status (5) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CTIF RNA expression–survival associations across cancer types. High CTIF expression shows unfavorable associations in BLCA, UVM, LUSC, ACC and THCA, but favorable associations in LGG. The BLCA 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 BLCA as the clearest survival context for CTIF RNA expression.
This table summarizes CTIF tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 11. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CTIF. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CTIF shows lower tumor expression in LUAD, THCA, BLCA, KICH and KIRP and higher tumor expression in LIHC. The LUAD box plot shows higher CTIF RNA expression in normal versus tumor tissue (log2 FC = −1.179, t-test p < 0.001).
This table shows molecular features associated with CTIF in patient tissues and cancer cell lines. In patient samples, CTIF shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, CTIF RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BONE.
