Q-omics provides the consensus-scored TLR2 profile across patient tissues and cancer cell-line models. TLR2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, TLR2 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, TLR2 protein abundance shows 32,880 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight MESO, KIRC, and GBM as cancer lineages where TLR2 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 TLR2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TLR2 survival associations across molecular data types. TLR2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (5) 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 TLR2 RNA expression–survival associations across cancer types. High TLR2 expression shows unfavorable associations in LGG and KICH, but favorable associations in MESO, SKCM, LUAD and CESC. The MESO Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify MESO as the clearest survival context for TLR2 RNA expression.
This table summarizes TLR2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 9. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TLR2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TLR2 shows lower tumor expression in LUAD and LUSC and higher tumor expression in KIRC, THCA, HNSC and STAD. The KIRC box plot shows higher TLR2 RNA expression in tumor versus normal tissue (log2 FC = +1.777, t-test p < 0.001).
This table shows molecular features associated with TLR2 in patient tissues and cancer cell lines. In patient samples, TLR2 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, TLR2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and BLOOD_Leukemia.
