Q-omics provides the consensus-scored TRAF2 profile across patient tissues and cancer cell-line models. TRAF2 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, TRAF2 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, TRAF2 protein abundance shows 24,406 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight ACC, KIRC, and GBM as cancer lineages where TRAF2 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 TRAF2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TRAF2 survival associations across molecular data types. TRAF2 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (2) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TRAF2 RNA expression–survival associations across cancer types. High TRAF2 expression shows unfavorable associations in ACC, KIRC, MESO, LIHC, UVM and LGG. The ACC 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 ACC as the clearest survival context for TRAF2 RNA expression.
This table summarizes TRAF2 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 8. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TRAF2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TRAF2 shows higher tumor expression in KIRC, HNSC, BLCA, COAD, KIRP and STAD. The KIRC box plot shows higher TRAF2 RNA expression in tumor versus normal tissue (log2 FC = +1.180, t-test p < 0.001).
This table shows molecular features associated with TRAF2 in patient tissues and cancer cell lines. In patient samples, TRAF2 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, TRAF2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BLOOD_Leukemia.
