Q-omics provides the consensus-scored FEM1A profile across patient tissues and cancer cell-line models. FEM1A expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, FEM1A is differentially expressed in 10, with the highest sampling consensus in THCA. Additionally, FEM1A RNA expression shows 19,050 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight HNSC, THCA, and ACC as cancer lineages where FEM1A 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 FEM1A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FEM1A survival associations across molecular data types. FEM1A RNA expression shows survival associations in the most cancer types (20), followed by mutation status (6) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FEM1A RNA expression–survival associations across cancer types. High FEM1A expression shows unfavorable associations in ACC and LUAD, but favorable associations in HNSC, KIRC, KIRP and THYM. The HNSC 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 HNSC as the clearest survival context for FEM1A RNA expression.
This table summarizes FEM1A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 2. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for FEM1A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FEM1A shows lower tumor expression in THCA, BRCA and LUAD and higher tumor expression in KIRC, LIHC and KICH. The THCA box plot shows higher FEM1A RNA expression in normal versus tumor tissue (log2 FC = −0.459, t-test p < 0.001).
This table shows molecular features associated with FEM1A in patient tissues and cancer cell lines. In patient samples, FEM1A 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, FEM1A RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and BLOOD_Leukemia.
