Q-omics provides the consensus-scored ATRX profile across patient tissues and cancer cell-line models. ATRX expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ATRX is differentially expressed in 7, with the highest sampling consensus in LIHC. Additionally, ATRX RNA expression shows 21,260 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, LIHC, and THYM as cancer lineages where ATRX 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 ATRX — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ATRX survival associations across molecular data types. ATRX RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) 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 ATRX RNA expression–survival associations across cancer types. High ATRX expression shows unfavorable associations in UVM and KICH, but favorable associations in KIRC, SKCM, SCLC and PCPG. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for ATRX RNA expression.
This table summarizes ATRX tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7, while mass-spec protein shows differences in 5. The strongest signals are observed in LIHC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for ATRX. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ATRX shows lower tumor expression in THCA and UCEC and higher tumor expression in LIHC, HNSC, CHOL and COAD. The LIHC box plot shows higher ATRX RNA expression in tumor versus normal tissue (log2 FC = +0.914, t-test p < 0.001).
This table shows molecular features associated with ATRX in patient tissues and cancer cell lines. In patient samples, ATRX shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, ATRX RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Leukemia.
