Q-omics provides the consensus-scored FLI1 profile across patient tissues and cancer cell-line models. FLI1 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, FLI1 is differentially expressed in 14, with the highest sampling consensus in LUAD. Additionally, FLI1 RNA expression shows 26,940 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight HNSC, LUAD, and LSCC as cancer lineages where FLI1 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 FLI1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FLI1 survival associations across molecular data types. FLI1 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (6) 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 FLI1 RNA expression–survival associations across cancer types. High FLI1 expression shows unfavorable associations in UVM and KIRP, but favorable associations in HNSC, KIRC, SKCM and LUAD. 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 FLI1 RNA expression.
This table summarizes FLI1 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 4. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for FLI1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FLI1 shows lower tumor expression in LUAD, BLCA, KICH, COAD and LUSC and higher tumor expression in KIRC. The LUAD box plot shows higher FLI1 RNA expression in normal versus tumor tissue (log2 FC = −2.008, t-test p < 0.001).
This table shows molecular features associated with FLI1 in patient tissues and cancer cell lines. In patient samples, FLI1 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, FLI1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and SOFT_TISSUE.
