Q-omics provides the consensus-scored FPGT-TNNI3K profile across patient tissues and cancer cell-line models. FPGT-TNNI3K expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, FPGT-TNNI3K is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, FPGT-TNNI3K RNA expression shows 19,069 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight HNSC, COAD, and UVM as cancer lineages where FPGT-TNNI3K 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-TNNI3K — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FPGT-TNNI3K survival associations across molecular data types. FPGT-TNNI3K RNA expression shows survival associations in the most cancer types (19), followed by mutation status (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FPGT-TNNI3K RNA expression–survival associations across cancer types. High FPGT-TNNI3K expression shows unfavorable associations in UVM, but favorable associations in HNSC, MESO, BRCA, KIRP and LIHC. The HNSC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify HNSC as the clearest survival context for FPGT-TNNI3K RNA expression.
This table summarizes FPGT-TNNI3K tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14. The strongest signals are observed in COAD for RNA.
This table ranks reproducible tumor–normal expression differences for FPGT-TNNI3K. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FPGT-TNNI3K shows lower tumor expression in COAD, LUSC, KICH, BRCA, UCEC and BLCA. The COAD box plot shows higher FPGT-TNNI3K RNA expression in normal versus tumor tissue (log2 FC = −0.084, t-test p < 0.001).
This table shows molecular features associated with FPGT-TNNI3K in patient tissues and cancer cell lines. In patient samples, FPGT-TNNI3K 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-TNNI3K RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
