Q-omics provides the consensus-scored ATF6 profile across patient tissues and cancer cell-line models. ATF6 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, ATF6 is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, ATF6 RNA expression shows 20,260 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight BLCA, HNSC, and ACC as cancer lineages where ATF6 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 ATF6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ATF6 survival associations across molecular data types. ATF6 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (8) 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 ATF6 RNA expression–survival associations across cancer types. High ATF6 expression shows unfavorable associations in BLCA, ACC, MESO and CESC, but favorable associations in KIRC and UCS. The BLCA 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 BLCA as the clearest survival context for ATF6 RNA expression.
This table summarizes ATF6 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 3. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for ATF6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ATF6 shows lower tumor expression in KICH and higher tumor expression in HNSC, LIHC, BRCA, BLCA and STAD. The HNSC box plot shows higher ATF6 RNA expression in tumor versus normal tissue (log2 FC = +0.492, t-test p < 0.001).
This table shows molecular features associated with ATF6 in patient tissues and cancer cell lines. In patient samples, ATF6 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, ATF6 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Lymphoma.
