Q-omics provides the consensus-scored POLD1 profile across patient tissues and cancer cell-line models. POLD1 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, POLD1 is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, POLD1 protein abundance shows 26,333 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, HNSC, and LSCC as cancer lineages where POLD1 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 POLD1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes POLD1 survival associations across molecular data types. POLD1 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (9) 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 POLD1 RNA expression–survival associations across cancer types. High POLD1 expression shows unfavorable associations in MESO, ACC, KIRC, LIHC and LGG, but favorable associations in SCLC. The MESO 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 MESO as the clearest survival context for POLD1 RNA expression.
This table summarizes POLD1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 8. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for POLD1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. POLD1 shows higher tumor expression in HNSC, KIRP, BLCA, COAD, KIRC and LIHC. The HNSC box plot shows higher POLD1 RNA expression in tumor versus normal tissue (log2 FC = +1.356, t-test p < 0.001).
This table shows molecular features associated with POLD1 in patient tissues and cancer cell lines. In patient samples, POLD1 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, POLD1 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 OVARY and SOFT_TISSUE.
