Q-omics provides the consensus-scored AMD1 profile across patient tissues and cancer cell-line models. AMD1 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, AMD1 is differentially expressed in 8, with the highest sampling consensus in THCA. Additionally, AMD1 RNA expression shows 20,094 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, THCA, and ACC as cancer lineages where AMD1 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 AMD1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes AMD1 survival associations across molecular data types. AMD1 RNA expression shows survival associations in the most cancer types (22), followed by mutation status (5) 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 AMD1 RNA expression–survival associations across cancer types. High AMD1 expression shows unfavorable associations in LIHC and BRCA, but favorable associations in KIRC, SKCM, UCS and READ. 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 AMD1 RNA expression.
This table summarizes AMD1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8, while mass-spec protein shows differences in 6. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for AMD1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. AMD1 shows lower tumor expression in THCA, KICH and KIRP and higher tumor expression in LIHC, CHOL and UCEC. The THCA box plot shows higher AMD1 RNA expression in normal versus tumor tissue (log2 FC = −0.974, t-test p < 0.001).
This table shows molecular features associated with AMD1 in patient tissues and cancer cell lines. In patient samples, AMD1 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, AMD1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LUNG_SCLC.
