DNA polymerase delta interacting protein 2Genealiases: PDIP38 · p38
Q-omics provides the consensus-scored POLDIP2 profile across patient tissues and cancer cell-line models. POLDIP2 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in SKCM. Among the 18 cancer types available for tumor–normal comparison, POLDIP2 is differentially expressed in 16, with the highest sampling consensus in KICH. Additionally, POLDIP2 protein abundance shows 28,877 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight SKCM, KICH, and LSCC as cancer lineages where POLDIP2 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 POLDIP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes POLDIP2 survival associations across molecular data types. POLDIP2 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (2) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible POLDIP2 RNA expression–survival associations across cancer types. High POLDIP2 expression shows unfavorable associations in SKCM, KICH, BLCA, LAML and HNSC, but favorable associations in LUSC. The SKCM 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 SKCM as the clearest survival context for POLDIP2 RNA expression.
This table summarizes POLDIP2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for POLDIP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. POLDIP2 shows lower tumor expression in KICH and higher tumor expression in BLCA, HNSC, LUAD, LIHC and COAD. The KICH box plot shows higher POLDIP2 RNA expression in normal versus tumor tissue (log2 FC = −1.229, t-test p < 0.001).
This table shows molecular features associated with POLDIP2 in patient tissues and cancer cell lines. In patient samples, POLDIP2 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, POLDIP2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in UPPER_AERODIGESTIVE_TRACT, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and SKIN.
