Q-omics provides the consensus-scored PARD3 profile across patient tissues and cancer cell-line models. PARD3 expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in BLCA. Among the 18 cancer types available for tumor–normal comparison, PARD3 is differentially expressed in 11, with the highest sampling consensus in LIHC. Additionally, PARD3 RNA expression shows 19,807 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight BLCA, LIHC, and ACC as cancer lineages where PARD3 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 PARD3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PARD3 survival associations across molecular data types. PARD3 RNA expression shows survival associations in the most cancer types (29), followed by mutation status (5) 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 PARD3 RNA expression–survival associations across cancer types. High PARD3 expression shows unfavorable associations in BLCA, ACC, LIHC, MESO and PAAD, but favorable associations in KIRC. The BLCA 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 BLCA as the clearest survival context for PARD3 RNA expression.
This table summarizes PARD3 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 6. The strongest signals are observed in LIHC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PARD3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PARD3 shows lower tumor expression in KICH and BRCA and higher tumor expression in LIHC, LUSC, KIRP and LUAD. The LIHC box plot shows higher PARD3 RNA expression in tumor versus normal tissue (log2 FC = +0.960, t-test p < 0.001).
This table shows molecular features associated with PARD3 in patient tissues and cancer cell lines. In patient samples, PARD3 shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, PARD3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OVARY, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Leukemia.
