Q-omics provides the consensus-scored TTLL4 profile across patient tissues and cancer cell-line models. TTLL4 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, TTLL4 is differentially expressed in 15, with the highest sampling consensus in COAD. Additionally, TTLL4 RNA expression shows 19,757 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRP, and COAD as cancer lineages where TTLL4 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 TTLL4 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TTLL4 survival associations across molecular data types. TTLL4 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (10) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TTLL4 RNA expression–survival associations across cancer types. High TTLL4 expression shows unfavorable associations in KIRP, LIHC, KIRC and KICH, but favorable associations in SCLC and UCS. The KIRP 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 KIRP as the clearest survival context for TTLL4 RNA expression.
This table summarizes TTLL4 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 2. The strongest signals are observed in KIRP for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for TTLL4. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TTLL4 shows lower tumor expression in KICH and higher tumor expression in COAD, KIRP, LIHC, BLCA and STAD. The COAD box plot shows higher TTLL4 RNA expression in tumor versus normal tissue (log2 FC = +1.289, t-test p < 0.001).
This table shows molecular features associated with TTLL4 in patient tissues and cancer cell lines. In patient samples, TTLL4 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, TTLL4 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in OVARY and BLOOD_Lymphoma.
