Q-omics provides the consensus-scored ATRN profile across patient tissues and cancer cell-line models. ATRN expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, ATRN is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, ATRN RNA expression shows 20,742 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight MESO, HNSC, and THYM as cancer lineages where ATRN 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 ATRN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ATRN survival associations across molecular data types. ATRN RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ATRN RNA expression–survival associations across cancer types. High ATRN expression shows unfavorable associations in MESO, BLCA and UVM, but favorable associations in KIRC, READ and UCS. The MESO Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .003). Together, the overview and detailed table identify MESO as the clearest survival context for ATRN RNA expression.
This table summarizes ATRN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for ATRN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ATRN shows lower tumor expression in KIRC and THCA and higher tumor expression in HNSC, BLCA, LIHC and LUSC. The HNSC box plot shows higher ATRN RNA expression in tumor versus normal tissue (log2 FC = +1.047, t-test p < 0.001).
This table shows molecular features associated with ATRN in patient tissues and cancer cell lines. In patient samples, ATRN 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, ATRN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in STOMACH, while CRISPR and shRNA rows add functional-dependency signals in SKIN and LARGE_INTESTINE.
