Q-omics provides the consensus-scored JPT2 profile across patient tissues and cancer cell-line models. JPT2 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, JPT2 is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, JPT2 protein abundance shows 21,409 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight MESO, HNSC, and PDAC as cancer lineages where JPT2 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 JPT2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes JPT2 survival associations across molecular data types. JPT2 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (2) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible JPT2 RNA expression–survival associations across cancer types. High JPT2 expression shows unfavorable associations in MESO, ACC, UVM, PAAD, LGG and LUAD. The MESO 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 MESO as the clearest survival context for JPT2 RNA expression.
This table summarizes JPT2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for JPT2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. JPT2 shows lower tumor expression in KICH and higher tumor expression in HNSC, KIRC, KIRP, LUAD and STAD. The HNSC box plot shows higher JPT2 RNA expression in tumor versus normal tissue (log2 FC = +1.062, t-test p < 0.001).
This table shows molecular features associated with JPT2 in patient tissues and cancer cell lines. In patient samples, JPT2 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, JPT2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in SKIN and BLOOD_Leukemia.
