Q-omics provides the consensus-scored FOLR3 profile across patient tissues and cancer cell-line models. FOLR3 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in THCA. Among the 18 cancer types available for tumor–normal comparison, FOLR3 is differentially expressed in 9, with the highest sampling consensus in HNSC. Additionally, FOLR3 protein abundance shows 25,363 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight THCA, HNSC, and GBM as cancer lineages where FOLR3 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 FOLR3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FOLR3 survival associations across molecular data types. FOLR3 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (8) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible FOLR3 RNA expression–survival associations across cancer types. High FOLR3 expression shows unfavorable associations in THCA, STAD, KIRC, ACC, GBM and MESO. The THCA 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 THCA as the clearest survival context for FOLR3 RNA expression.
This table summarizes FOLR3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 9. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for FOLR3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FOLR3 shows lower tumor expression in KIRC, KIRP, LUAD, THCA and LUSC and higher tumor expression in HNSC. The HNSC box plot shows higher FOLR3 RNA expression in tumor versus normal tissue (log2 FC = +4.158, t-test p < 0.001).
This table shows molecular features associated with FOLR3 in patient tissues and cancer cell lines. In patient samples, FOLR3 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, FOLR3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LARGE_INTESTINE.