Q-omics provides the consensus-scored FAM166A profile across patient tissues and cancer cell-line models. FAM166A expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, FAM166A is differentially expressed in 9, with the highest sampling consensus in UCEC. Additionally, FAM166A RNA expression shows 13,541 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight COAD, UCEC, and KIRP as cancer lineages where FAM166A 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 FAM166A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FAM166A survival associations across molecular data types. FAM166A RNA expression shows survival associations in the most cancer types (22), followed by mutation status (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FAM166A RNA expression–survival associations across cancer types. High FAM166A expression shows unfavorable associations in COAD, ACC, UVM and UCS, but favorable associations in PAAD and UCEC. The COAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify COAD as the clearest survival context for FAM166A RNA expression.
This table summarizes FAM166A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9. The strongest signals are observed in UCEC for RNA.
This table ranks reproducible tumor–normal expression differences for FAM166A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FAM166A shows lower tumor expression in KICH and THCA and higher tumor expression in UCEC, STAD, COAD and LIHC. The UCEC box plot shows higher FAM166A RNA expression in tumor versus normal tissue (log2 FC = +0.347, t-test p = .006).
This table shows molecular features associated with FAM166A in patient tissues and cancer cell lines. In patient samples, FAM166A shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, FAM166A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and SOFT_TISSUE.
