Q-omics provides the consensus-scored FSTL4 profile across patient tissues and cancer cell-line models. FSTL4 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, FSTL4 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, FSTL4 protein abundance shows 21,510 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight UVM, KIRC, and LUAD as cancer lineages where FSTL4 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 FSTL4 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FSTL4 survival associations across molecular data types. FSTL4 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (11) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FSTL4 RNA expression–survival associations across cancer types. High FSTL4 expression shows unfavorable associations in UVM, DLBC and STAD, but favorable associations in MESO, KIRC and HNSC. 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 FSTL4 RNA expression.
This table summarizes FSTL4 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 KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for FSTL4. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FSTL4 shows lower tumor expression in KIRC, KIRP and KICH and higher tumor expression in UCEC, HNSC and LIHC. The KIRC box plot shows higher FSTL4 RNA expression in normal versus tumor tissue (log2 FC = −1.470, t-test p < 0.001).
This table shows molecular features associated with FSTL4 in patient tissues and cancer cell lines. In patient samples, FSTL4 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, FSTL4 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Lymphoma, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BREAST.
