Q-omics provides the consensus-scored AFM profile across patient tissues and cancer cell-line models. AFM expression is associated with patient survival in 17 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, AFM is differentially expressed in 11, with the highest sampling consensus in KIRC. Additionally, AFM protein abundance shows 23,045 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, and LSCC as cancer lineages where AFM 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 AFM — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes AFM survival associations across molecular data types. AFM RNA expression shows survival associations in the most cancer types (17), followed by mutation status (7) 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 AFM RNA expression–survival associations across cancer types. High AFM expression shows unfavorable associations in MESO, CHOL, COAD and LUAD, but favorable associations in KIRC and LIHC. 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 AFM RNA expression.
This table summarizes AFM tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for AFM. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. AFM shows lower tumor expression in KIRC, KIRP, LIHC, KICH and CHOL and higher tumor expression in LUAD. The KIRC box plot shows higher AFM RNA expression in normal versus tumor tissue (log2 FC = −2.652, t-test p < 0.001).
This table shows molecular features associated with AFM in patient tissues and cancer cell lines. In patient samples, AFM 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, AFM RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Leukemia.
