Q-omics provides the consensus-scored PRDX6 profile across patient tissues and cancer cell-line models. PRDX6 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PRDX6 is differentially expressed in 8, with the highest sampling consensus in COAD. Additionally, PRDX6 protein abundance shows 24,361 significant protein co-abundance associations, with the highest sampling consensus in PDAC. Together, these results highlight KIRP, COAD, and PDAC as cancer lineages where PRDX6 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 PRDX6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRDX6 survival associations across molecular data types. PRDX6 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (5) 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 PRDX6 RNA expression–survival associations across cancer types. High PRDX6 expression shows unfavorable associations in KIRP, HNSC, BLCA, LUAD, ACC and LGG. The KIRP 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 KIRP as the clearest survival context for PRDX6 RNA expression.
This table summarizes PRDX6 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 7. The strongest signals are observed in COAD for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PRDX6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRDX6 shows lower tumor expression in COAD, KICH and BRCA and higher tumor expression in KIRP, LIHC and BLCA. The COAD box plot shows higher PRDX6 RNA expression in normal versus tumor tissue (log2 FC = −1.696, t-test p < 0.001).
This table shows molecular features associated with PRDX6 in patient tissues and cancer cell lines. In patient samples, PRDX6 shows the broadest associations at the RNA and protein expression levels, with PDAC recurring as the lineage with the largest associated feature set. In cancer cell lines, PRDX6 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in STOMACH, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and LUNG_SCLC.
