Q-omics provides the consensus-scored FUT3 profile across patient tissues and cancer cell-line models. FUT3 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, FUT3 is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, FUT3 RNA expression shows 12,551 significant gene co-expression associations, with the highest sampling consensus in ESCA. Together, these results highlight KIRC, HNSC, and ESCA as cancer lineages where FUT3 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 FUT3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FUT3 survival associations across molecular data types. FUT3 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (5) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FUT3 RNA expression–survival associations across cancer types. High FUT3 expression shows unfavorable associations in BRCA, ACC, KICH and ESCA, but favorable associations in KIRC and UVM. 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 FUT3 RNA expression.
This table summarizes FUT3 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 HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for FUT3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FUT3 shows lower tumor expression in HNSC, KICH, KIRP and KIRC and higher tumor expression in LUAD and THCA. The HNSC box plot shows higher FUT3 RNA expression in normal versus tumor tissue (log2 FC = −2.628, t-test p < 0.001).
This table shows molecular features associated with FUT3 in patient tissues and cancer cell lines. In patient samples, FUT3 shows the broadest associations at the RNA and protein expression levels, with ESCA recurring as the lineage with the largest associated feature set. In cancer cell lines, FUT3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and LUNG_NSCLC_LUAD.
