Q-omics provides the consensus-scored PRLHR profile across patient tissues and cancer cell-line models. PRLHR expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, PRLHR is differentially expressed in 7, with the highest sampling consensus in UCEC. Additionally, PRLHR RNA expression shows 8,458 significant gene co-expression associations, with the highest sampling consensus in PCPG. Together, these results highlight COAD, UCEC, and PCPG as cancer lineages where PRLHR 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 PRLHR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRLHR survival associations across molecular data types. PRLHR RNA expression shows survival associations in the most cancer types (21), followed by mutation status (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRLHR RNA expression–survival associations across cancer types. High PRLHR expression shows unfavorable associations in COAD, BLCA and BRCA, but favorable associations in LGG, UCEC and CESC. The COAD 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 COAD as the clearest survival context for PRLHR RNA expression.
This table summarizes PRLHR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 7. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for PRLHR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRLHR shows lower tumor expression in UCEC, STAD, PRAD, BLCA and BRCA and higher tumor expression in KIRC. The UCEC box plot shows higher PRLHR RNA expression in normal versus tumor tissue (log2 FC = −1.544, t-test p < 0.001).
This table shows molecular features associated with PRLHR in patient tissues and cancer cell lines. In patient samples, PRLHR shows the broadest associations at the RNA and protein expression levels, with PCPG recurring as the lineage with the largest associated feature set. In cancer cell lines, PRLHR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.