Q-omics provides the consensus-scored JUP profile across patient tissues and cancer cell-line models. JUP expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, JUP is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, JUP protein abundance shows 25,502 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, KIRC, and LSCC as cancer lineages where JUP 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 JUP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes JUP survival associations across molecular data types. JUP RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible JUP RNA expression–survival associations across cancer types. High JUP expression shows unfavorable associations in LGG and SKCM, but favorable associations in UVM, KIRC, SCLC and LUSC. The UVM 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 UVM as the clearest survival context for JUP RNA expression.
This table summarizes JUP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for JUP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. JUP shows lower tumor expression in KIRC and KICH and higher tumor expression in LUSC, BLCA, LUAD and HNSC. The KIRC box plot shows higher JUP RNA expression in normal versus tumor tissue (log2 FC = −1.219, t-test p < 0.001).
This table shows molecular features associated with JUP in patient tissues and cancer cell lines. In patient samples, JUP 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, JUP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and BONE.
