Q-omics provides the consensus-scored MFSD9 profile across patient tissues and cancer cell-line models. MFSD9 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, MFSD9 is differentially expressed in 15, with the highest sampling consensus in LUAD. Additionally, MFSD9 RNA expression shows 20,212 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight UVM, and LUAD as cancer lineages where MFSD9 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 MFSD9 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MFSD9 survival associations across molecular data types. MFSD9 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MFSD9 RNA expression–survival associations across cancer types. High MFSD9 expression shows unfavorable associations in UVM, ACC, KICH and LGG, but favorable associations in KIRC and UCS. 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 MFSD9 RNA expression.
This table summarizes MFSD9 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 1. The strongest signals are observed in LUAD for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for MFSD9. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MFSD9 shows lower tumor expression in THCA and higher tumor expression in LUAD, BLCA, HNSC, STAD and LUSC. The LUAD box plot shows higher MFSD9 RNA expression in tumor versus normal tissue (log2 FC = +1.235, t-test p < 0.001).
This table shows molecular features associated with MFSD9 in patient tissues and cancer cell lines. In patient samples, MFSD9 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, MFSD9 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BREAST and UPPER_AERODIGESTIVE_TRACT.
