Q-omics provides the consensus-scored ATAD5 profile across patient tissues and cancer cell-line models. ATAD5 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, ATAD5 is differentially expressed in 16, with the highest sampling consensus in BLCA. Additionally, ATAD5 RNA expression shows 24,959 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, BLCA, and LSCC as cancer lineages where ATAD5 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 ATAD5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ATAD5 survival associations across molecular data types. ATAD5 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (9) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ATAD5 RNA expression–survival associations across cancer types. High ATAD5 expression shows unfavorable associations in ACC, MESO, KIRC, LIHC and KIRP, but favorable associations in UCS. 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 ATAD5 RNA expression.
This table summarizes ATAD5 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 4. The strongest signals are observed in HNSC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for ATAD5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ATAD5 shows higher tumor expression in BLCA, HNSC, KIRC, STAD, LUAD and KIRP. The BLCA box plot shows higher ATAD5 RNA expression in tumor versus normal tissue (log2 FC = +1.838, t-test p < 0.001).
This table shows molecular features associated with ATAD5 in patient tissues and cancer cell lines. In patient samples, ATAD5 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, ATAD5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
