Q-omics provides the consensus-scored PTH1R profile across patient tissues and cancer cell-line models. PTH1R expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PTH1R is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, PTH1R RNA expression shows 22,852 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, KIRC, and LSCC as cancer lineages where PTH1R 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 PTH1R — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTH1R survival associations across molecular data types. PTH1R RNA expression shows survival associations in the most cancer types (24), followed by mutation status (6) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PTH1R RNA expression–survival associations across cancer types. High PTH1R expression shows unfavorable associations in COAD, LUSC, STAD and BLCA, but favorable associations in KIRP and KIRC. The KIRP 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 KIRP as the clearest survival context for PTH1R RNA expression.
This table summarizes PTH1R 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 1. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PTH1R. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTH1R shows lower tumor expression in KIRC, KICH, KIRP, BLCA, LUAD and COAD. The KIRC box plot shows higher PTH1R RNA expression in normal versus tumor tissue (log2 FC = −3.229, t-test p < 0.001).
This table shows molecular features associated with PTH1R in patient tissues and cancer cell lines. In patient samples, PTH1R 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, PTH1R RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and LARGE_INTESTINE.
