Q-omics provides the consensus-scored FLRT3 profile across patient tissues and cancer cell-line models. FLRT3 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, FLRT3 is differentially expressed in 14, with the highest sampling consensus in KICH. Additionally, FLRT3 protein abundance shows 21,469 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, KICH, and LSCC as cancer lineages where FLRT3 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 FLRT3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes FLRT3 survival associations across molecular data types. FLRT3 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (7) 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 FLRT3 RNA expression–survival associations across cancer types. High FLRT3 expression shows unfavorable associations in PAAD, LUSC and UCEC, but favorable associations in KIRC, UCS and MESO. The KIRC Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify KIRC as the clearest survival context for FLRT3 RNA expression.
This table summarizes FLRT3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for FLRT3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. FLRT3 shows lower tumor expression in KICH, LUAD, KIRC and LUSC and higher tumor expression in HNSC and BLCA. The KICH box plot shows higher FLRT3 RNA expression in normal versus tumor tissue (log2 FC = −5.203, t-test p < 0.001).
This table shows molecular features associated with FLRT3 in patient tissues and cancer cell lines. In patient samples, FLRT3 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, FLRT3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in SKIN and LARGE_INTESTINE.
