Q-omics provides the consensus-scored PTRH2 profile across patient tissues and cancer cell-line models. PTRH2 expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PTRH2 is differentially expressed in 17, with the highest sampling consensus in KIRC. Additionally, PTRH2 RNA expression shows 18,887 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRP, KIRC, and ACC as cancer lineages where PTRH2 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 PTRH2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTRH2 survival associations across molecular data types. PTRH2 RNA expression shows survival associations in the most cancer types (26), followed by mutation status (4) 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 PTRH2 RNA expression–survival associations across cancer types. High PTRH2 expression shows unfavorable associations in KIRP, UVM, LIHC, ACC, SCLC and KIRC. 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 PTRH2 RNA expression.
This table summarizes PTRH2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 17, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for PTRH2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTRH2 shows higher tumor expression in KIRC, BLCA, KIRP, LIHC, STAD and LUAD. The KIRC box plot shows higher PTRH2 RNA expression in tumor versus normal tissue (log2 FC = +0.771, t-test p < 0.001).
This table shows molecular features associated with PTRH2 in patient tissues and cancer cell lines. In patient samples, PTRH2 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, PTRH2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LUNG_SCLC.
