Q-omics provides the consensus-scored PGD profile across patient tissues and cancer cell-line models. PGD expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, PGD is differentially expressed in 14, with the highest sampling consensus in THCA. Additionally, PGD RNA expression shows 18,856 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight ACC, and THCA as cancer lineages where PGD 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 PGD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PGD survival associations across molecular data types. PGD RNA expression shows survival associations in the most cancer types (24), followed by mutation status (6) 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 PGD RNA expression–survival associations across cancer types. High PGD expression shows unfavorable associations in ACC, LIHC, LGG, BLCA and LUAD, but favorable associations in SCLC. 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 PGD RNA expression.
This table summarizes PGD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in THCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PGD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PGD shows lower tumor expression in THCA and KIRC and higher tumor expression in COAD, LIHC, BLCA and LUSC. The THCA box plot shows higher PGD RNA expression in normal versus tumor tissue (log2 FC = −0.854, t-test p < 0.001).
This table shows molecular features associated with PGD in patient tissues and cancer cell lines. In patient samples, PGD 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, PGD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in URINARY_TRACT and LARGE_INTESTINE.
