Q-omics provides the consensus-scored TFAP4 profile across patient tissues and cancer cell-line models. TFAP4 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LIHC. Among the 18 cancer types available for tumor–normal comparison, TFAP4 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, TFAP4 RNA expression shows 21,874 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight LIHC, KIRC, and LSCC as cancer lineages where TFAP4 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 TFAP4 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TFAP4 survival associations across molecular data types. TFAP4 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TFAP4 RNA expression–survival associations across cancer types. High TFAP4 expression shows unfavorable associations in LIHC, KIRP, ACC and KIRC, but favorable associations in READ and HNSC. The LIHC 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 LIHC as the clearest survival context for TFAP4 RNA expression.
This table summarizes TFAP4 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 4. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TFAP4. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TFAP4 shows higher tumor expression in KIRC, COAD, BLCA, KIRP, STAD and LIHC. The KIRC box plot shows higher TFAP4 RNA expression in tumor versus normal tissue (log2 FC = +0.536, t-test p < 0.001).
This table shows molecular features associated with TFAP4 in patient tissues and cancer cell lines. In patient samples, TFAP4 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, TFAP4 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUSC, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and BONE.
