Q-omics provides the consensus-scored CTCFL profile across patient tissues and cancer cell-line models. CTCFL expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, CTCFL is differentially expressed in 7, with the highest sampling consensus in KICH. Additionally, CTCFL protein abundance shows 25,020 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, KICH, and LSCC as cancer lineages where CTCFL 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 CTCFL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CTCFL survival associations across molecular data types. CTCFL RNA expression shows survival associations in the most cancer types (19), followed by mutation status (7) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible CTCFL RNA expression–survival associations across cancer types. High CTCFL expression shows unfavorable associations in UVM, LUAD, ACC, LUSC and UCEC, but favorable associations in UCS. The UVM 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 UVM as the clearest survival context for CTCFL RNA expression.
This table summarizes CTCFL tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 6. The strongest signals are observed in KICH for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CTCFL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CTCFL shows lower tumor expression in KICH, BRCA, THCA and KIRC and higher tumor expression in HNSC and LUSC. The KICH box plot shows higher CTCFL RNA expression in normal versus tumor tissue (log2 FC = −0.032, t-test p < 0.001).
This table shows molecular features associated with CTCFL in patient tissues and cancer cell lines. In patient samples, CTCFL shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, CTCFL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BREAST and LARGE_INTESTINE.
