pancreatic lipase related protein 3Genealiases: []
Q-omics provides the consensus-scored PNLIPRP3 profile across patient tissues and cancer cell-line models. PNLIPRP3 expression is associated with patient survival in 18 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PNLIPRP3 is differentially expressed in 8, with the highest sampling consensus in COAD. Additionally, PNLIPRP3 RNA expression shows 11,224 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight KIRC, COAD, and HNSC as cancer lineages where PNLIPRP3 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 PNLIPRP3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PNLIPRP3 survival associations across molecular data types. PNLIPRP3 RNA expression shows survival associations in the most cancer types (18), 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 PNLIPRP3 RNA expression–survival associations across cancer types. High PNLIPRP3 expression shows unfavorable associations in KIRC, UVM, MESO, READ and LUSC, but favorable associations in ACC. The KIRC 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 KIRC as the clearest survival context for PNLIPRP3 RNA expression.
This table summarizes PNLIPRP3 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 1. The strongest signals are observed in COAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PNLIPRP3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PNLIPRP3 shows lower tumor expression in COAD and THCA and higher tumor expression in BLCA, KICH, LUAD and KIRP. The COAD box plot shows higher PNLIPRP3 RNA expression in normal versus tumor tissue (log2 FC = −0.087, t-test p < 0.001).
This table shows molecular features associated with PNLIPRP3 in patient tissues and cancer cell lines. In patient samples, PNLIPRP3 shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, PNLIPRP3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BLOOD_Myeloma, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and UPPER_AERODIGESTIVE_TRACT.
