Q-omics provides the consensus-scored MFSD4A profile across patient tissues and cancer cell-line models. MFSD4A expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, MFSD4A is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, MFSD4A RNA expression shows 20,446 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRC, and KIRP as cancer lineages where MFSD4A 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 MFSD4A — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MFSD4A survival associations across molecular data types. MFSD4A RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MFSD4A RNA expression–survival associations across cancer types. High MFSD4A expression shows unfavorable associations in UVM, but favorable associations in KIRC, BRCA, HNSC, CESC and KICH. 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 MFSD4A RNA expression.
This table summarizes MFSD4A tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 4. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MFSD4A. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MFSD4A shows lower tumor expression in KIRC, KIRP, KICH, LUSC and COAD and higher tumor expression in THCA. The KIRC box plot shows higher MFSD4A RNA expression in normal versus tumor tissue (log2 FC = −4.526, t-test p < 0.001).
This table shows molecular features associated with MFSD4A in patient tissues and cancer cell lines. In patient samples, MFSD4A shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, MFSD4A 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 SOFT_TISSUE and BLOOD_Leukemia.
