Q-omics provides the consensus-scored PRSS3 profile across patient tissues and cancer cell-line models. PRSS3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, PRSS3 is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, PRSS3 RNA expression shows 16,165 significant protein co-abundance associations, with the highest sampling consensus in GBM. Together, these results highlight KICH, HNSC, and GBM as cancer lineages where PRSS3 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 PRSS3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRSS3 survival associations across molecular data types. PRSS3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRSS3 RNA expression–survival associations across cancer types. High PRSS3 expression shows unfavorable associations in KICH, UCEC, KIRP and MESO, but favorable associations in LAML and OV. The KICH Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .003). Together, the overview and detailed table identify KICH as the clearest survival context for PRSS3 RNA expression.
This table summarizes PRSS3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 1. The strongest signals are observed in HNSC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for PRSS3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRSS3 shows lower tumor expression in HNSC, KIRC and KIRP and higher tumor expression in LUAD, THCA and LUSC. The HNSC box plot shows higher PRSS3 RNA expression in normal versus tumor tissue (log2 FC = −2.909, t-test p < 0.001).
This table shows molecular features associated with PRSS3 in patient tissues and cancer cell lines. In patient samples, PRSS3 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, PRSS3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in OESOPHAGUS, while CRISPR and shRNA rows add functional-dependency signals in OVARY and BLOOD_Lymphoma.
