Q-omics provides the consensus-scored PTGIR profile across patient tissues and cancer cell-line models. PTGIR expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, PTGIR is differentially expressed in 11, with the highest sampling consensus in HNSC. Additionally, PTGIR RNA expression shows 21,662 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, HNSC, and LSCC as cancer lineages where PTGIR 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 PTGIR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTGIR survival associations across molecular data types. PTGIR RNA expression shows survival associations in the most cancer types (24), followed by mutation status (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PTGIR RNA expression–survival associations across cancer types. High PTGIR expression shows unfavorable associations in UVM, KIRP, LUSC, LGG and BRCA, but favorable associations in HNSC. The UVM Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify UVM as the clearest survival context for PTGIR RNA expression.
This table summarizes PTGIR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11. The strongest signals are observed in HNSC for RNA.
This table ranks reproducible tumor–normal expression differences for PTGIR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTGIR shows lower tumor expression in THCA, KICH, LUAD, LUSC and KIRP and higher tumor expression in HNSC. The HNSC box plot shows higher PTGIR RNA expression in tumor versus normal tissue (log2 FC = +0.752, t-test p < 0.001).
This table shows molecular features associated with PTGIR in patient tissues and cancer cell lines. In patient samples, PTGIR 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, PTGIR 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 UPPER_AERODIGESTIVE_TRACT and BLOOD_Leukemia.
