Q-omics provides the consensus-scored AMH profile across patient tissues and cancer cell-line models. AMH expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, AMH is differentially expressed in 16, with the highest sampling consensus in COAD. Additionally, AMH RNA expression shows 15,454 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, COAD, and ACC as cancer lineages where AMH 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 AMH — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes AMH survival associations across molecular data types. AMH RNA expression shows survival associations in the most cancer types (26), 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 AMH RNA expression–survival associations across cancer types. High AMH expression shows unfavorable associations in KIRC, MESO, ACC, KIRP, BRCA and LUAD. 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 AMH RNA expression.
This table summarizes AMH 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 1. The strongest signals are observed in BLCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for AMH. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. AMH shows higher tumor expression in COAD, BLCA, HNSC, STAD, KIRC and UCEC. The COAD box plot shows higher AMH RNA expression in tumor versus normal tissue (log2 FC = +2.564, t-test p < 0.001).
This table shows molecular features associated with AMH in patient tissues and cancer cell lines. In patient samples, AMH 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, AMH 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 BREAST and BLOOD_Leukemia.
