Q-omics provides the consensus-scored FEM1B profile across patient tissues and cancer cell-line models. FEM1B expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, FEM1B is differentially expressed in 11, with the highest sampling consensus in THCA. Additionally, FEM1B RNA expression shows 21,116 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, THCA, and ACC as cancer lineages where FEM1B 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 FEM1B — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FEM1B survival associations across molecular data types. FEM1B RNA expression shows survival associations in the most cancer types (21), followed by mutation status (4) 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 FEM1B RNA expression–survival associations across cancer types. High FEM1B expression shows unfavorable associations in UVM, ACC and KICH, but favorable associations in KIRC, SCLC and BRCA. 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 FEM1B RNA expression.
This table summarizes FEM1B 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 3. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for FEM1B. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FEM1B shows lower tumor expression in THCA, UCEC and COAD and higher tumor expression in HNSC, LIHC and CHOL. The THCA box plot shows higher FEM1B RNA expression in normal versus tumor tissue (log2 FC = −0.537, t-test p < 0.001).
This table shows molecular features associated with FEM1B in patient tissues and cancer cell lines. In patient samples, FEM1B 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, FEM1B 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 LUNG_SCLC and LARGE_INTESTINE.
