Q-omics provides the consensus-scored PTGDR profile across patient tissues and cancer cell-line models. PTGDR expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, PTGDR is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, PTGDR RNA expression shows 18,077 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, COAD, and LSCC as cancer lineages where PTGDR 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 PTGDR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTGDR survival associations across molecular data types. PTGDR RNA expression shows survival associations in the most cancer types (27), 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 PTGDR RNA expression–survival associations across cancer types. High PTGDR expression shows unfavorable associations in KIRP and UVM, but favorable associations in SKCM, UCEC, ACC and LIHC. The SKCM 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 SKCM as the clearest survival context for PTGDR RNA expression.
This table summarizes PTGDR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14. The strongest signals are observed in COAD for RNA.
This table ranks reproducible tumor–normal expression differences for PTGDR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTGDR shows lower tumor expression in COAD, THCA, LUSC and UCEC and higher tumor expression in KIRC and HNSC. The COAD box plot shows higher PTGDR RNA expression in normal versus tumor tissue (log2 FC = −2.744, t-test p < 0.001).
This table shows molecular features associated with PTGDR in patient tissues and cancer cell lines. In patient samples, PTGDR 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, PTGDR RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in LIVER and LARGE_INTESTINE.
