junction mediating and regulatory protein, p53 cofactorGenealiases: WHAMM2 · WHDC1L3
Q-omics provides the consensus-scored JMY profile across patient tissues and cancer cell-line models. JMY expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in OV. Among the 18 cancer types available for tumor–normal comparison, JMY is differentially expressed in 9, with the highest sampling consensus in KIRC. Additionally, JMY RNA expression shows 20,410 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight OV, KIRC, and THYM as cancer lineages where JMY 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 JMY — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes JMY survival associations across molecular data types. JMY RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible JMY RNA expression–survival associations across cancer types. High JMY expression shows unfavorable associations in OV, but favorable associations in HNSC, KIRC, LGG, SKCM and LIHC. The OV Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p < 0.001). Together, the overview and detailed table identify OV as the clearest survival context for JMY RNA expression.
This table summarizes JMY 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 LSCC for protein.
This table ranks reproducible tumor–normal expression differences for JMY. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. JMY shows lower tumor expression in KIRC, BLCA and BRCA and higher tumor expression in HNSC, LIHC and CHOL. The KIRC box plot shows higher JMY RNA expression in normal versus tumor tissue (log2 FC = −1.170, t-test p < 0.001).
This table shows molecular features associated with JMY in patient tissues and cancer cell lines. In patient samples, JMY shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, JMY 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 LIVER and LARGE_INTESTINE.
