Q-omics provides the consensus-scored MEPCE profile across patient tissues and cancer cell-line models. MEPCE expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, MEPCE is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, MEPCE protein abundance shows 29,826 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRC, HNSC, and LSCC as cancer lineages where MEPCE 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 MEPCE — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MEPCE survival associations across molecular data types. MEPCE RNA expression shows survival associations in the most cancer types (25), 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 MEPCE RNA expression–survival associations across cancer types. High MEPCE expression shows unfavorable associations in UCEC, MESO, LIHC, LUAD and COAD, but favorable associations in KIRC. 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 MEPCE RNA expression.
This table summarizes MEPCE tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 6. The strongest signals are observed in HNSC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for MEPCE. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MEPCE shows lower tumor expression in THCA and UCEC and higher tumor expression in HNSC, COAD, LIHC and STAD. The HNSC box plot shows higher MEPCE RNA expression in tumor versus normal tissue (log2 FC = +0.934, t-test p < 0.001).
This table shows molecular features associated with MEPCE in patient tissues and cancer cell lines. In patient samples, MEPCE 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, MEPCE RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in CNS and UPPER_AERODIGESTIVE_TRACT.
