Q-omics provides the consensus-scored PDZK1 profile across patient tissues and cancer cell-line models. PDZK1 expression is associated with patient survival in 23 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PDZK1 is differentially expressed in 8, with the highest sampling consensus in KICH. Additionally, PDZK1 RNA expression shows 20,394 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KIRC, KICH, and UVM as cancer lineages where PDZK1 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 PDZK1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDZK1 survival associations across molecular data types. PDZK1 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (1) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PDZK1 RNA expression–survival associations across cancer types. High PDZK1 expression shows unfavorable associations in MESO, ACC and LGG, but favorable associations in KIRC, BRCA and READ. 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 PDZK1 RNA expression.
This table summarizes PDZK1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8, while mass-spec protein shows differences in 2. The strongest signals are observed in KICH for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PDZK1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDZK1 shows lower tumor expression in KICH, KIRP and COAD and higher tumor expression in BLCA, LIHC and HNSC. The KICH box plot shows higher PDZK1 RNA expression in normal versus tumor tissue (log2 FC = −6.153, t-test p < 0.001).
This table shows molecular features associated with PDZK1 in patient tissues and cancer cell lines. In patient samples, PDZK1 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, PDZK1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUSC, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Leukemia.
