Q-omics provides the consensus-scored JPH1 profile across patient tissues and cancer cell-line models. JPH1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, JPH1 is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, JPH1 protein abundance shows 37,415 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRP, COAD, and GBM as cancer lineages where JPH1 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 JPH1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes JPH1 survival associations across molecular data types. JPH1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (10) 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 JPH1 RNA expression–survival associations across cancer types. High JPH1 expression shows unfavorable associations in KIRP, UVM, UCEC and MESO, but favorable associations in LUSC and LUAD. The KIRP 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 KIRP as the clearest survival context for JPH1 RNA expression.
This table summarizes JPH1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 9. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for JPH1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. JPH1 shows lower tumor expression in LUAD and KIRC and higher tumor expression in COAD, THCA, STAD and KIRP. The COAD box plot shows higher JPH1 RNA expression in tumor versus normal tissue (log2 FC = +2.174, t-test p < 0.001).
This table shows molecular features associated with JPH1 in patient tissues and cancer cell lines. In patient samples, JPH1 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, JPH1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in BONE and LARGE_INTESTINE.
