Q-omics provides the consensus-scored ATMIN profile across patient tissues and cancer cell-line models. ATMIN expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, ATMIN is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, ATMIN RNA expression shows 20,037 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight BLCA, HNSC, and ACC as cancer lineages where ATMIN 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 ATMIN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ATMIN survival associations across molecular data types. ATMIN RNA expression shows survival associations in the most cancer types (19), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ATMIN RNA expression–survival associations across cancer types. High ATMIN expression shows unfavorable associations in BLCA, PAAD, MESO and ACC, but favorable associations in KIRC and CHOL. 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 ATMIN RNA expression.
This table summarizes ATMIN 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 1. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for ATMIN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ATMIN shows lower tumor expression in THCA and higher tumor expression in HNSC, LUAD, LUSC, CHOL and LIHC. The HNSC box plot shows higher ATMIN RNA expression in tumor versus normal tissue (log2 FC = +0.373, t-test p < 0.001).
This table shows molecular features associated with ATMIN in patient tissues and cancer cell lines. In patient samples, ATMIN 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, ATMIN 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 UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
