Q-omics provides the consensus-scored FKTN profile across patient tissues and cancer cell-line models. FKTN expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, FKTN is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, FKTN RNA expression shows 21,441 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight BLCA, HNSC, and ACC as cancer lineages where FKTN 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 FKTN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FKTN survival associations across molecular data types. FKTN RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FKTN RNA expression–survival associations across cancer types. High FKTN expression shows unfavorable associations in BLCA, ACC, MESO, LIHC and LUAD, but favorable associations in KIRC. The BLCA 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 BLCA as the clearest survival context for FKTN RNA expression.
This table summarizes FKTN 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 2. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for FKTN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FKTN shows lower tumor expression in THCA and higher tumor expression in HNSC, STAD, LIHC, BRCA and LUAD. The HNSC box plot shows higher FKTN RNA expression in tumor versus normal tissue (log2 FC = +0.852, t-test p < 0.001).
This table shows molecular features associated with FKTN in patient tissues and cancer cell lines. In patient samples, FKTN 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, FKTN 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 OESOPHAGUS and BLOOD_Leukemia.
