Q-omics provides the consensus-scored FIGN profile across patient tissues and cancer cell-line models. FIGN expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in CESC. Among the 18 cancer types available for tumor–normal comparison, FIGN is differentially expressed in 14, with the highest sampling consensus in KIRP. Additionally, FIGN RNA expression shows 18,475 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight CESC, KIRP, and UVM as cancer lineages where FIGN 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 FIGN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FIGN survival associations across molecular data types. FIGN RNA expression shows survival associations in the most cancer types (22), followed by mutation status (10) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FIGN RNA expression–survival associations across cancer types. High FIGN expression shows unfavorable associations in CESC, HNSC, LIHC, UCEC, LUSC and ACC. The CESC 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 CESC as the clearest survival context for FIGN RNA expression.
This table summarizes FIGN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRP for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for FIGN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FIGN shows lower tumor expression in COAD, BRCA, THCA and KICH and higher tumor expression in KIRP and KIRC. The KIRP box plot shows higher FIGN RNA expression in tumor versus normal tissue (log2 FC = +1.521, t-test p < 0.001).
This table shows molecular features associated with FIGN in patient tissues and cancer cell lines. In patient samples, FIGN shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, FIGN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in CNS and UPPER_AERODIGESTIVE_TRACT.
