Q-omics provides the consensus-scored AMOT profile across patient tissues and cancer cell-line models. AMOT expression is associated with patient survival in 16 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, AMOT is differentially expressed in 10, with the highest sampling consensus in COAD. Additionally, AMOT RNA expression shows 19,747 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, COAD, and THYM as cancer lineages where AMOT 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 AMOT — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes AMOT survival associations across molecular data types. AMOT RNA expression shows survival associations in the most cancer types (16), followed by mutation status (8) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible AMOT RNA expression–survival associations across cancer types. High AMOT expression shows unfavorable associations in ACC and TGCT, but favorable associations in KIRC, LUAD, KIRP and UVM. 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 AMOT RNA expression.
This table summarizes AMOT 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 6. The strongest signals are observed in COAD for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for AMOT. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. AMOT shows lower tumor expression in HNSC, BRCA, KICH and BLCA and higher tumor expression in COAD and THCA. The COAD box plot shows higher AMOT RNA expression in tumor versus normal tissue (log2 FC = +0.875, t-test p < 0.001).
This table shows molecular features associated with AMOT in patient tissues and cancer cell lines. In patient samples, AMOT shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, AMOT RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
