Q-omics provides the consensus-scored AMACR profile across patient tissues and cancer cell-line models. AMACR expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, AMACR is differentially expressed in 10, with the highest sampling consensus in KIRP. Additionally, AMACR RNA expression shows 19,126 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and KIRP as cancer lineages where AMACR 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 AMACR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes AMACR survival associations across molecular data types. AMACR RNA expression shows survival associations in the most cancer types (21), followed by mutation status (5) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible AMACR RNA expression–survival associations across cancer types. High AMACR expression shows unfavorable associations in UVM and KICH, but favorable associations in PAAD, KIRC, ESCA and KIRP. The UVM Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify UVM as the clearest survival context for AMACR RNA expression.
This table summarizes AMACR 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 5. The strongest signals are observed in BRCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for AMACR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. AMACR shows lower tumor expression in CHOL and KICH and higher tumor expression in KIRP, BRCA, LUAD and KIRC. The KIRP box plot shows higher AMACR RNA expression in tumor versus normal tissue (log2 FC = +2.242, t-test p < 0.001).
This table shows molecular features associated with AMACR in patient tissues and cancer cell lines. In patient samples, AMACR shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, AMACR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Lymphoma.
