Q-omics provides the consensus-scored PKP2 profile across patient tissues and cancer cell-line models. PKP2 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, PKP2 is differentially expressed in 10, with the highest sampling consensus in THCA. Additionally, PKP2 protein abundance shows 21,058 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KIRC, THCA, and GBM as cancer lineages where PKP2 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 PKP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PKP2 survival associations across molecular data types. PKP2 RNA expression shows survival associations in the most cancer types (23), followed by mutation status (5) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PKP2 RNA expression–survival associations across cancer types. High PKP2 expression shows unfavorable associations in LUAD, MESO and CESC, but favorable associations in KIRC, READ 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 PKP2 RNA expression.
This table summarizes PKP2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 6. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PKP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PKP2 shows lower tumor expression in COAD and higher tumor expression in THCA, LUAD, LUSC, STAD and BLCA. The THCA box plot shows higher PKP2 RNA expression in tumor versus normal tissue (log2 FC = +1.372, t-test p < 0.001).
This table shows molecular features associated with PKP2 in patient tissues and cancer cell lines. In patient samples, PKP2 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, PKP2 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 LUNG_NSCLC_LUAD and BONE.
