Q-omics provides the consensus-scored TFPI2 profile across patient tissues and cancer cell-line models. TFPI2 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, TFPI2 is differentially expressed in 12, with the highest sampling consensus in KICH. Additionally, TFPI2 RNA expression shows 16,069 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight UVM, KICH, and THYM as cancer lineages where TFPI2 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 TFPI2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes TFPI2 survival associations across molecular data types. TFPI2 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (4) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible TFPI2 RNA expression–survival associations across cancer types. High TFPI2 expression shows unfavorable associations in UVM, LUSC, OV and LGG, but favorable associations in BRCA and SKCM. The UVM 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 UVM as the clearest survival context for TFPI2 RNA expression.
This table summarizes TFPI2 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 4. The strongest signals are observed in BRCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for TFPI2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. TFPI2 shows lower tumor expression in KICH, BRCA, LIHC and BLCA and higher tumor expression in KIRP and LUAD. The KICH box plot shows higher TFPI2 RNA expression in normal versus tumor tissue (log2 FC = −3.402, t-test p < 0.001).
This table shows molecular features associated with TFPI2 in patient tissues and cancer cell lines. In patient samples, TFPI2 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, TFPI2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in CNS, while CRISPR and shRNA rows add functional-dependency signals in LIVER and BREAST.
