Q-omics provides the consensus-scored PDGFD profile across patient tissues and cancer cell-line models. PDGFD expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PDGFD is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, PDGFD RNA expression shows 19,713 significant protein co-abundance associations, with the highest sampling consensus in BRCA. Together, these results highlight KIRC, and BRCA as cancer lineages where PDGFD 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 PDGFD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDGFD survival associations across molecular data types. PDGFD RNA expression shows survival associations in the most cancer types (21), followed by mutation status (5) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PDGFD RNA expression–survival associations across cancer types. High PDGFD expression shows unfavorable associations in BLCA, STAD and LGG, but favorable associations in KIRC, SKCM and LIHC. The KIRC 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 KIRC as the clearest survival context for PDGFD RNA expression.
This table summarizes PDGFD 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 3. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PDGFD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDGFD shows lower tumor expression in COAD, KICH, BLCA, UCEC and BRCA and higher tumor expression in KIRC. The KIRC box plot shows higher PDGFD RNA expression in tumor versus normal tissue (log2 FC = +2.182, t-test p < 0.001).
This table shows molecular features associated with PDGFD in patient tissues and cancer cell lines. In patient samples, PDGFD shows the broadest associations at the RNA and protein expression levels, with BRCA recurring as the lineage with the largest associated feature set. In cancer cell lines, PDGFD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BLOOD_Lymphoma.
