Q-omics provides the consensus-scored TTLL3 profile across patient tissues and cancer cell-line models. TTLL3 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TTLL3 is differentially expressed in 11, with the highest sampling consensus in LIHC. Additionally, TTLL3 RNA expression shows 19,788 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, LIHC, and UVM as cancer lineages where TTLL3 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 TTLL3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TTLL3 survival associations across molecular data types. TTLL3 RNA expression shows survival associations in the most cancer types (21), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TTLL3 RNA expression–survival associations across cancer types. High TTLL3 expression shows unfavorable associations in KIRC, LGG and PRAD, but favorable associations in HNSC, BLCA and SKCM. The KIRC 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 KIRC as the clearest survival context for TTLL3 RNA expression.
This table summarizes TTLL3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 1. The strongest signals are observed in LIHC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TTLL3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TTLL3 shows lower tumor expression in LUSC, BRCA and KICH and higher tumor expression in LIHC, COAD and KIRC. The LIHC box plot shows higher TTLL3 RNA expression in tumor versus normal tissue (log2 FC = +0.645, t-test p < 0.001).
This table shows molecular features associated with TTLL3 in patient tissues and cancer cell lines. In patient samples, TTLL3 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, TTLL3 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 LARGE_INTESTINE and UPPER_AERODIGESTIVE_TRACT.
