Q-omics provides the consensus-scored ATR profile across patient tissues and cancer cell-line models. ATR 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, ATR is differentially expressed in 13, with the highest sampling consensus in COAD. Additionally, ATR RNA expression shows 21,106 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and COAD as cancer lineages where ATR 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 ATR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ATR survival associations across molecular data types. ATR RNA expression shows survival associations in the most cancer types (24), followed by mutation status (10) 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 ATR RNA expression–survival associations across cancer types. High ATR expression shows unfavorable associations in ACC, LGG, LIHC, PAAD and UCEC, but favorable associations in HNSC. 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 ATR RNA expression.
This table summarizes ATR 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 3. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for ATR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ATR shows lower tumor expression in THCA and higher tumor expression in COAD, HNSC, LIHC, BLCA and STAD. The COAD box plot shows higher ATR RNA expression in tumor versus normal tissue (log2 FC = +0.915, t-test p < 0.001).
This table shows molecular features associated with ATR in patient tissues and cancer cell lines. In patient samples, ATR 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, ATR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Leukemia.
