Q-omics provides the consensus-scored ACBD5 profile across patient tissues and cancer cell-line models. ACBD5 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, ACBD5 is differentially expressed in 10, with the highest sampling consensus in BLCA. Additionally, ACBD5 protein abundance shows 33,946 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, BLCA, and LUAD as cancer lineages where ACBD5 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 ACBD5 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes ACBD5 survival associations across molecular data types. ACBD5 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (7) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible ACBD5 RNA expression–survival associations across cancer types. High ACBD5 expression shows unfavorable associations in ESCA, UVM and BRCA, but favorable associations in KIRC, LGG and SKCM. 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 ACBD5 RNA expression.
This table summarizes ACBD5 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 11. The strongest signals are observed in BLCA for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for ACBD5. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. ACBD5 shows lower tumor expression in KICH, THCA and KIRC and higher tumor expression in BLCA, STAD and BRCA. The BLCA box plot shows higher ACBD5 RNA expression in tumor versus normal tissue (log2 FC = +0.876, t-test p < 0.001).
This table shows molecular features associated with ACBD5 in patient tissues and cancer cell lines. In patient samples, ACBD5 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, ACBD5 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and UPPER_AERODIGESTIVE_TRACT.
