Q-omics provides the consensus-scored TTN profile across patient tissues and cancer cell-line models. TTN expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in LUSC. Among the 18 cancer types available for tumor–normal comparison, TTN is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, TTN RNA expression shows 19,458 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight LUSC, KIRC, and UVM as cancer lineages where TTN 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 TTN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TTN survival associations across molecular data types. TTN RNA expression shows survival associations in the most cancer types (21), followed by mutation status (20) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TTN RNA expression–survival associations across cancer types. High TTN expression shows unfavorable associations in LUSC, KIRC, ACC, UVM and STAD, but favorable associations in GBM. The LUSC 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 LUSC as the clearest survival context for TTN RNA expression.
This table summarizes TTN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TTN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TTN shows lower tumor expression in HNSC, LUSC and LUAD and higher tumor expression in KIRC, CHOL and KIRP. The KIRC box plot shows higher TTN RNA expression in tumor versus normal tissue (log2 FC = +0.129, t-test p < 0.001).
This table shows molecular features associated with TTN in patient tissues and cancer cell lines. In patient samples, TTN 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, TTN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and UPPER_AERODIGESTIVE_TRACT.
