Q-omics provides the consensus-scored CTTN profile across patient tissues and cancer cell-line models. CTTN expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, CTTN is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, CTTN protein abundance shows 20,136 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight HNSC, and LUAD as cancer lineages where CTTN 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 CTTN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CTTN survival associations across molecular data types. CTTN RNA expression shows survival associations in the most cancer types (27), followed by mutation status (6) 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 CTTN RNA expression–survival associations across cancer types. High CTTN expression shows unfavorable associations in HNSC, CESC, PAAD, LIHC, LGG and KICH. The HNSC 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 HNSC as the clearest survival context for CTTN RNA expression.
This table summarizes CTTN 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 9. The strongest signals are observed in THCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for CTTN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CTTN shows higher tumor expression in HNSC, THCA, LIHC, LUAD, KIRP and BLCA. The HNSC box plot shows higher CTTN RNA expression in tumor versus normal tissue (log2 FC = +0.949, t-test p < 0.001).
This table shows molecular features associated with CTTN in patient tissues and cancer cell lines. In patient samples, CTTN shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, CTTN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BREAST and SOFT_TISSUE.
