Q-omics provides the consensus-scored ATF6B profile across patient tissues and cancer cell-line models. ATF6B expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, ATF6B is differentially expressed in 13, with the highest sampling consensus in HNSC. Additionally, ATF6B RNA expression shows 19,332 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight COAD, HNSC, and ACC as cancer lineages where ATF6B 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 ATF6B — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ATF6B survival associations across molecular data types. ATF6B RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ATF6B RNA expression–survival associations across cancer types. High ATF6B expression shows unfavorable associations in COAD, BRCA, LIHC, HNSC and LGG, but favorable associations in READ. The COAD 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 COAD as the clearest survival context for ATF6B RNA expression.
This table summarizes ATF6B tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 2. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for ATF6B. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ATF6B shows lower tumor expression in KICH and higher tumor expression in HNSC, LIHC, KIRC, STAD and BRCA. The HNSC box plot shows higher ATF6B RNA expression in tumor versus normal tissue (log2 FC = +0.704, t-test p < 0.001).
This table shows molecular features associated with ATF6B in patient tissues and cancer cell lines. In patient samples, ATF6B 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, ATF6B 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 BLOOD_Leukemia and UPPER_AERODIGESTIVE_TRACT.
