Q-omics provides the consensus-scored FPGT profile across patient tissues and cancer cell-line models. FPGT expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, FPGT is differentially expressed in 12, with the highest sampling consensus in THCA. Additionally, FPGT RNA expression shows 19,875 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, THCA, and UVM as cancer lineages where FPGT 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 FPGT — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FPGT survival associations across molecular data types. FPGT RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FPGT RNA expression–survival associations across cancer types. High FPGT expression shows unfavorable associations in LIHC, LGG, KICH and THCA, but favorable associations in KIRC and COAD. 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 FPGT RNA expression.
This table summarizes FPGT tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 5. The strongest signals are observed in THCA for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for FPGT. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FPGT shows lower tumor expression in THCA and KICH and higher tumor expression in LIHC, HNSC, BRCA and BLCA. The THCA box plot shows higher FPGT RNA expression in normal versus tumor tissue (log2 FC = −1.021, t-test p < 0.001).
This table shows molecular features associated with FPGT in patient tissues and cancer cell lines. In patient samples, FPGT 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, FPGT 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 URINARY_TRACT and UPPER_AERODIGESTIVE_TRACT.
