Q-omics provides the consensus-scored TFPI profile across patient tissues and cancer cell-line models. TFPI expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in STAD. Among the 18 cancer types available for tumor–normal comparison, TFPI is differentially expressed in 16, with the highest sampling consensus in THCA. Additionally, TFPI RNA expression shows 18,828 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight STAD, THCA, and KIRP as cancer lineages where TFPI 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 TFPI — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TFPI survival associations across molecular data types. TFPI RNA expression shows survival associations in the most cancer types (25), followed by mutation status (8) 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 TFPI RNA expression–survival associations across cancer types. High TFPI expression shows unfavorable associations in STAD, LUAD, LGG, CESC and LUSC, but favorable associations in PRAD. The STAD Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify STAD as the clearest survival context for TFPI RNA expression.
This table summarizes TFPI tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 5. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for TFPI. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TFPI shows lower tumor expression in THCA, KICH, UCEC and LUSC and higher tumor expression in KIRP and KIRC. The THCA box plot shows higher TFPI RNA expression in normal versus tumor tissue (log2 FC = −2.025, t-test p < 0.001).
This table shows molecular features associated with TFPI in patient tissues and cancer cell lines. In patient samples, TFPI shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, TFPI RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
