Q-omics provides the consensus-scored TLR8 profile across patient tissues and cancer cell-line models. TLR8 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, TLR8 is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, TLR8 protein abundance shows 23,546 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, KIRC, and LSCC as cancer lineages where TLR8 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 TLR8 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TLR8 survival associations across molecular data types. TLR8 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TLR8 RNA expression–survival associations across cancer types. High TLR8 expression shows unfavorable associations in UVM and LGG, but favorable associations in SKCM, HNSC, CESC and KIRC. The SKCM 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 SKCM as the clearest survival context for TLR8 RNA expression.
This table summarizes TLR8 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 8. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TLR8. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TLR8 shows lower tumor expression in LUSC and LUAD and higher tumor expression in KIRC, HNSC, KIRP and THCA. The KIRC box plot shows higher TLR8 RNA expression in tumor versus normal tissue (log2 FC = +1.940, t-test p < 0.001).
This table shows molecular features associated with TLR8 in patient tissues and cancer cell lines. In patient samples, TLR8 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, TLR8 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 OVARY and BLOOD_Leukemia.
