Q-omics provides the consensus-scored TREM2 profile across patient tissues and cancer cell-line models. TREM2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in DLBC. Among the 18 cancer types available for tumor–normal comparison, TREM2 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, TREM2 protein abundance shows 26,234 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight DLBC, KIRC, and LUAD as cancer lineages where TREM2 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 TREM2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TREM2 survival associations across molecular data types. TREM2 RNA expression shows survival associations in the most cancer types (24), 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 TREM2 RNA expression–survival associations across cancer types. High TREM2 expression shows unfavorable associations in LIHC, LGG and OV, but favorable associations in DLBC, SKCM and CESC. The DLBC 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 DLBC as the clearest survival context for TREM2 RNA expression.
This table summarizes TREM2 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 9. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TREM2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TREM2 shows higher tumor expression in KIRC, HNSC, KIRP, THCA, COAD and BLCA. The KIRC box plot shows higher TREM2 RNA expression in tumor versus normal tissue (log2 FC = +4.322, t-test p < 0.001).
This table shows molecular features associated with TREM2 in patient tissues and cancer cell lines. In patient samples, TREM2 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, TREM2 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 BLOOD_Leukemia and OVARY.
