Q-omics provides the consensus-scored TNFAIP3 profile across patient tissues and cancer cell-line models. TNFAIP3 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, TNFAIP3 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, TNFAIP3 protein abundance shows 22,500 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, KIRC, and LSCC as cancer lineages where TNFAIP3 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 TNFAIP3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TNFAIP3 survival associations across molecular data types. TNFAIP3 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TNFAIP3 RNA expression–survival associations across cancer types. High TNFAIP3 expression shows unfavorable associations in ACC, KIRP, LGG and LIHC, but favorable associations in ESCA and KIRC. 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 TNFAIP3 RNA expression.
This table summarizes TNFAIP3 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 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TNFAIP3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TNFAIP3 shows lower tumor expression in LUSC and UCEC and higher tumor expression in KIRC, HNSC, STAD and LIHC. The KIRC box plot shows higher TNFAIP3 RNA expression in tumor versus normal tissue (log2 FC = +1.716, t-test p < 0.001).
This table shows molecular features associated with TNFAIP3 in patient tissues and cancer cell lines. In patient samples, TNFAIP3 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, TNFAIP3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BREAST and LARGE_INTESTINE.
