Q-omics provides the consensus-scored EZHIP profile across patient tissues and cancer cell-line models. EZHIP expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, EZHIP is differentially expressed in 5, with the highest sampling consensus in KIRC. Additionally, EZHIP RNA expression shows 13,467 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, and TGCT as cancer lineages where EZHIP 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 EZHIP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes EZHIP survival associations across molecular data types. EZHIP RNA expression shows survival associations in the most cancer types (23), followed by mutation status (11) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible EZHIP RNA expression–survival associations across cancer types. High EZHIP expression shows unfavorable associations in KIRC, but favorable associations in HNSC, UCS, PAAD, SKCM and ESCA. The KIRC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify KIRC as the clearest survival context for EZHIP RNA expression.
This table summarizes EZHIP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 5, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for EZHIP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. EZHIP shows lower tumor expression in COAD, ESCA and LUSC and higher tumor expression in KIRC and LIHC. The KIRC box plot shows higher EZHIP RNA expression in tumor versus normal tissue (log2 FC = +0.081, t-test p < 0.001).
This table shows molecular features associated with EZHIP in patient tissues and cancer cell lines. In patient samples, EZHIP shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, EZHIP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia.
