Q-omics provides the consensus-scored PRDX3 profile across patient tissues and cancer cell-line models. PRDX3 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PRDX3 is differentially expressed in 11, with the highest sampling consensus in KICH. Additionally, PRDX3 protein abundance shows 24,568 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, KICH, and GBM as cancer lineages where PRDX3 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 PRDX3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRDX3 survival associations across molecular data types. PRDX3 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (4) and mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRDX3 RNA expression–survival associations across cancer types. High PRDX3 expression shows unfavorable associations in CESC, UVM and HNSC, but favorable associations in KIRC, COAD and SCLC. 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 PRDX3 RNA expression.
This table summarizes PRDX3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 7. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PRDX3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRDX3 shows lower tumor expression in KICH, THCA, KIRC and KIRP and higher tumor expression in LUAD and STAD. The KICH box plot shows higher PRDX3 RNA expression in normal versus tumor tissue (log2 FC = −2.155, t-test p < 0.001).
This table shows molecular features associated with PRDX3 in patient tissues and cancer cell lines. In patient samples, PRDX3 shows the broadest associations at the RNA and protein expression levels, with GBM recurring as the lineage with the largest associated feature set. In cancer cell lines, PRDX3 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 LUNG_NSCLC_LUAD and UPPER_AERODIGESTIVE_TRACT.
