Q-omics provides the consensus-scored MEFV profile across patient tissues and cancer cell-line models. MEFV expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, MEFV is differentially expressed in 9, with the highest sampling consensus in KIRC. Additionally, MEFV RNA expression shows 23,174 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, KIRC, and LSCC as cancer lineages where MEFV 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 MEFV — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MEFV survival associations across molecular data types. MEFV RNA expression shows survival associations in the most cancer types (25), followed by mutation status (11) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MEFV RNA expression–survival associations across cancer types. High MEFV expression shows unfavorable associations in KIRP, STAD, LAML and LGG, but favorable associations in SKCM and ESCA. The KIRP Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .008). Together, the overview and detailed table identify KIRP as the clearest survival context for MEFV RNA expression.
This table summarizes MEFV 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 4. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for MEFV. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MEFV shows lower tumor expression in LUAD, LUSC, LIHC and BRCA and higher tumor expression in KIRC and HNSC. The KIRC box plot shows higher MEFV RNA expression in tumor versus normal tissue (log2 FC = +0.871, t-test p < 0.001).
This table shows molecular features associated with MEFV in patient tissues and cancer cell lines. In patient samples, MEFV 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, MEFV RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and LARGE_INTESTINE.
