TLR4 interactor with leucine rich repeatsGenealiases: []
Q-omics provides the consensus-scored TRIL profile across patient tissues and cancer cell-line models. TRIL expression is associated with patient survival in 31 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, TRIL is differentially expressed in 11, with the highest sampling consensus in KICH. Additionally, TRIL RNA expression shows 18,525 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, KICH, and THYM as cancer lineages where TRIL 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 TRIL — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TRIL survival associations across molecular data types. TRIL RNA expression shows survival associations in the most cancer types (31), followed by mutation status (2) 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 TRIL RNA expression–survival associations across cancer types. High TRIL expression shows unfavorable associations in UVM, ACC and OV, but favorable associations in KIRC, SKCM and LAML. The KIRC 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 KIRC as the clearest survival context for TRIL RNA expression.
This table summarizes TRIL 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 3. The strongest signals are observed in KIRP for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for TRIL. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TRIL shows lower tumor expression in KICH, KIRP, HNSC, BLCA and UCEC and higher tumor expression in LIHC. The KICH box plot shows higher TRIL RNA expression in normal versus tumor tissue (log2 FC = −2.520, t-test p < 0.001).
This table shows molecular features associated with TRIL in patient tissues and cancer cell lines. In patient samples, TRIL shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, TRIL RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in SKIN.
