Q-omics provides the consensus-scored JUN profile across patient tissues and cancer cell-line models. JUN expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, JUN is differentially expressed in 11, with the highest sampling consensus in THCA. Additionally, JUN RNA expression shows 17,682 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and THCA as cancer lineages where JUN 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 JUN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes JUN survival associations across molecular data types. JUN RNA expression shows survival associations in the most cancer types (25), followed by mutation status (5) 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 JUN RNA expression–survival associations across cancer types. High JUN expression shows unfavorable associations in ACC, LGG, BLCA, ESCA and LUSC, but favorable associations in KIRC. The ACC 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 ACC as the clearest survival context for JUN RNA expression.
This table summarizes JUN 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 5. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for JUN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. JUN shows lower tumor expression in THCA, BLCA, KICH, UCEC, BRCA and LUSC. The THCA box plot shows higher JUN RNA expression in normal versus tumor tissue (log2 FC = −2.298, t-test p < 0.001).
This table shows molecular features associated with JUN in patient tissues and cancer cell lines. In patient samples, JUN 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, JUN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Lymphoma and LUNG_NSCLC_LUAD.
