Q-omics provides the consensus-scored PNLIPRP2 profile across patient tissues and cancer cell-line models. PNLIPRP2 expression is associated with patient survival in 16 of 34 cancer types, with the highest sampling consensus in UCEC. Among the 18 cancer types available for tumor–normal comparison, PNLIPRP2 is differentially expressed in 4, with the highest sampling consensus in COAD. Additionally, PNLIPRP2 RNA expression shows 11,671 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight UCEC, COAD, and TGCT as cancer lineages where PNLIPRP2 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 PNLIPRP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PNLIPRP2 survival associations across molecular data types. PNLIPRP2 RNA expression shows survival associations in the most cancer types (16), followed by mutation status (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PNLIPRP2 RNA expression–survival associations across cancer types. High PNLIPRP2 expression shows unfavorable associations in UCEC, LIHC, ACC, LUAD and KIRC, but favorable associations in UCS. The UCEC 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 UCEC as the clearest survival context for PNLIPRP2 RNA expression.
This table summarizes PNLIPRP2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 4, while mass-spec protein shows differences in 1. The strongest signals are observed in COAD for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for PNLIPRP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PNLIPRP2 shows lower tumor expression in COAD, READ and KICH and higher tumor expression in BRCA. The COAD box plot shows higher PNLIPRP2 RNA expression in normal versus tumor tissue (log2 FC = −1.560, t-test p < 0.001).
This table shows molecular features associated with PNLIPRP2 in patient tissues and cancer cell lines. In patient samples, PNLIPRP2 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, PNLIPRP2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BREAST.
