Q-omics provides the consensus-scored MFNG profile across patient tissues and cancer cell-line models. MFNG expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, MFNG is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, MFNG protein abundance shows 27,015 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight HNSC, KIRC, and LUAD as cancer lineages where MFNG 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 MFNG — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MFNG survival associations across molecular data types. MFNG RNA expression shows survival associations in the most cancer types (20), followed by mutation status (2) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MFNG RNA expression–survival associations across cancer types. High MFNG expression shows unfavorable associations in UVM and LGG, but favorable associations in HNSC, SKCM, UCEC and CESC. The HNSC 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 HNSC as the clearest survival context for MFNG RNA expression.
This table summarizes MFNG 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 8. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for MFNG. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MFNG shows lower tumor expression in COAD, LUSC, LUAD, KICH and UCEC and higher tumor expression in KIRC. The KIRC box plot shows higher MFNG RNA expression in tumor versus normal tissue (log2 FC = +1.361, t-test p < 0.001).
This table shows molecular features associated with MFNG in patient tissues and cancer cell lines. In patient samples, MFNG 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, MFNG RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Lymphoma.
