Q-omics provides the consensus-scored EMSY profile across patient tissues and cancer cell-line models. EMSY expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, EMSY is differentially expressed in 11, with the highest sampling consensus in THCA. Additionally, EMSY RNA expression shows 21,651 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, THCA, and ACC as cancer lineages where EMSY 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 EMSY — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EMSY survival associations across molecular data types. EMSY RNA expression shows survival associations in the most cancer types (24), followed by mutation status (7) 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 EMSY RNA expression–survival associations across cancer types. High EMSY expression shows unfavorable associations in ACC, KICH and MESO, but favorable associations in KIRC, HNSC and UCS. 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 EMSY RNA expression.
This table summarizes EMSY 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 4. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for EMSY. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EMSY shows lower tumor expression in THCA and higher tumor expression in HNSC, LIHC, BRCA, CHOL and STAD. The THCA box plot shows higher EMSY RNA expression in normal versus tumor tissue (log2 FC = −1.034, t-test p < 0.001).
This table shows molecular features associated with EMSY in patient tissues and cancer cell lines. In patient samples, EMSY shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, EMSY RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
