Q-omics provides the consensus-scored PTRH1 profile across patient tissues and cancer cell-line models. PTRH1 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, PTRH1 is differentially expressed in 11, with the highest sampling consensus in COAD. Additionally, PTRH1 RNA expression shows 18,588 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and COAD as cancer lineages where PTRH1 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 PTRH1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTRH1 survival associations across molecular data types. PTRH1 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (2) and mass-spec protein abundance (7). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PTRH1 RNA expression–survival associations across cancer types. High PTRH1 expression shows unfavorable associations in ACC, BLCA, KIRP, COAD and KIRC, but favorable associations in STAD. The ACC 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 ACC as the clearest survival context for PTRH1 RNA expression.
This table summarizes PTRH1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 3. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PTRH1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTRH1 shows lower tumor expression in LUAD, THCA and LUSC and higher tumor expression in COAD, HNSC and KIRC. The COAD box plot shows higher PTRH1 RNA expression in tumor versus normal tissue (log2 FC = +0.268, t-test p < 0.001).
This table shows molecular features associated with PTRH1 in patient tissues and cancer cell lines. In patient samples, PTRH1 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, PTRH1 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 BLOOD_Leukemia and SOFT_TISSUE.
