ATPase family AAA domain containing 3AGenealiases: HAYOS · PHRINL
Q-omics provides the consensus-scored ATAD3A profile across patient tissues and cancer cell-line models. ATAD3A expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ATAD3A is differentially expressed in 16, with the highest sampling consensus in COAD. Additionally, ATAD3A protein abundance shows 19,623 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, COAD, and LSCC as cancer lineages where ATAD3A 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 ATAD3A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ATAD3A survival associations across molecular data types. ATAD3A RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ATAD3A RNA expression–survival associations across cancer types. High ATAD3A expression shows unfavorable associations in KIRC, ACC, BLCA, KICH, LGG and LIHC. The KIRC 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 KIRC as the clearest survival context for ATAD3A RNA expression.
This table summarizes ATAD3A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for ATAD3A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ATAD3A shows higher tumor expression in COAD, BLCA, STAD, KIRP, LUAD and LUSC. The COAD box plot shows higher ATAD3A RNA expression in tumor versus normal tissue (log2 FC = +1.742, t-test p < 0.001).
This table shows molecular features associated with ATAD3A in patient tissues and cancer cell lines. In patient samples, ATAD3A shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, ATAD3A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Lymphoma.
