Q-omics provides the consensus-scored AMELX profile across patient tissues and cancer cell-line models. AMELX expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, AMELX is differentially expressed in 5, with the highest sampling consensus in COAD. Additionally, AMELX RNA expression shows 14,261 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, COAD, and LSCC as cancer lineages where AMELX 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 AMELX — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes AMELX survival associations across molecular data types. AMELX RNA expression shows survival associations in the most cancer types (22), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible AMELX RNA expression–survival associations across cancer types. High AMELX expression shows unfavorable associations in KIRC, KIRP, CESC, BRCA and THCA, but favorable associations in SCLC. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .003). Together, the overview and detailed table identify KIRC as the clearest survival context for AMELX RNA expression.
This table summarizes AMELX tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 5, while mass-spec protein shows differences in 1. The strongest signals are observed in COAD for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for AMELX. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. AMELX shows lower tumor expression in THCA and LUSC and higher tumor expression in COAD, STAD and LIHC. The COAD box plot shows higher AMELX RNA expression in tumor versus normal tissue (log2 FC = +1.069, t-test p < 0.001).
This table shows molecular features associated with AMELX in patient tissues and cancer cell lines. In patient samples, AMELX 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, AMELX 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_Myeloma and CNS.
