Q-omics provides the consensus-scored PRSS22 profile across patient tissues and cancer cell-line models. PRSS22 expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, PRSS22 is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, PRSS22 RNA expression shows 13,922 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, and THYM as cancer lineages where PRSS22 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 PRSS22 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRSS22 survival associations across molecular data types. PRSS22 RNA expression shows survival associations in the most cancer types (20), followed by mutation status (2) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRSS22 RNA expression–survival associations across cancer types. High PRSS22 expression shows unfavorable associations in KIRC, BRCA, MESO, GBM and LUSC, but favorable associations in UCS. 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 PRSS22 RNA expression.
This table summarizes PRSS22 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PRSS22. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRSS22 shows lower tumor expression in KIRC and KIRP and higher tumor expression in COAD, THCA, BLCA and LUAD. The KIRC box plot shows higher PRSS22 RNA expression in normal versus tumor tissue (log2 FC = −2.807, t-test p < 0.001).
This table shows molecular features associated with PRSS22 in patient tissues and cancer cell lines. In patient samples, PRSS22 shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, PRSS22 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and LARGE_INTESTINE.
