Q-omics provides the consensus-scored TTR profile across patient tissues and cancer cell-line models. TTR expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, TTR is differentially expressed in 12, with the highest sampling consensus in KIRP. Additionally, TTR protein abundance shows 32,807 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight LIHC, KIRP, and HNSC as cancer lineages where TTR 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 TTR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TTR survival associations across molecular data types. TTR RNA expression shows survival associations in the most cancer types (21), followed by mutation status (3) 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 TTR RNA expression–survival associations across cancer types. High TTR expression shows unfavorable associations in UVM, LGG, HNSC and KIRP, but favorable associations in LIHC and PAAD. The LIHC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify LIHC as the clearest survival context for TTR RNA expression.
This table summarizes TTR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TTR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TTR shows lower tumor expression in KIRP, KIRC, COAD, THCA, LIHC and CHOL. The KIRP box plot shows higher TTR RNA expression in normal versus tumor tissue (log2 FC = −1.840, t-test p < 0.001).
This table shows molecular features associated with TTR in patient tissues and cancer cell lines. In patient samples, TTR shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, TTR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and LIVER.
