family with sequence similarity 66 member AGenealiases: []
Q-omics provides the consensus-scored FAM66A profile across patient tissues and cancer cell-line models. FAM66A expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, FAM66A is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, FAM66A RNA expression shows 16,098 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight COAD, KIRC, and TGCT as cancer lineages where FAM66A 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 FAM66A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FAM66A survival associations across molecular data types. FAM66A RNA expression shows survival associations in the most cancer types (21), followed by mutation status (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FAM66A RNA expression–survival associations across cancer types. High FAM66A expression shows unfavorable associations in COAD, MESO, KIRP, DLBC and LIHC, but favorable associations in ACC. The COAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify COAD as the clearest survival context for FAM66A RNA expression.
This table summarizes FAM66A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for FAM66A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FAM66A shows lower tumor expression in KIRC, KICH, BRCA, THCA and HNSC and higher tumor expression in CHOL. The KIRC box plot shows higher FAM66A RNA expression in normal versus tumor tissue (log2 FC = −0.285, t-test p < 0.001).
This table shows molecular features associated with FAM66A in patient tissues and cancer cell lines. In patient samples, FAM66A shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set.
