Q-omics provides the consensus-scored PRSS16 profile across patient tissues and cancer cell-line models. PRSS16 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in OV. Among the 18 cancer types available for tumor–normal comparison, PRSS16 is differentially expressed in 9, with the highest sampling consensus in THCA. Additionally, PRSS16 RNA expression shows 16,804 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight OV, THCA, and KIRP as cancer lineages where PRSS16 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 PRSS16 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRSS16 survival associations across molecular data types. PRSS16 RNA expression shows survival associations in the most cancer types (27), 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 PRSS16 RNA expression–survival associations across cancer types. High PRSS16 expression shows favorable associations in OV, SKCM, READ, MESO, BLCA and KIRC. The OV 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 OV as the clearest survival context for PRSS16 RNA expression.
This table summarizes PRSS16 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 2. The strongest signals are observed in THCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for PRSS16. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRSS16 shows lower tumor expression in THCA and higher tumor expression in BLCA, HNSC, LUAD, CHOL and KIRC. The THCA box plot shows higher PRSS16 RNA expression in normal versus tumor tissue (log2 FC = −1.622, t-test p < 0.001).
This table shows molecular features associated with PRSS16 in patient tissues and cancer cell lines. In patient samples, PRSS16 shows the broadest associations at the RNA and protein expression levels, with KIRP recurring as the lineage with the largest associated feature set. In cancer cell lines, PRSS16 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 BLOOD_Leukemia and SOFT_TISSUE.
