Q-omics provides the consensus-scored PRSS42P profile across patient tissues and cancer cell-line models. PRSS42P expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in COAD. Among the 18 cancer types available for tumor–normal comparison, PRSS42P is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, PRSS42P RNA expression shows 15,522 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight COAD, KIRC, and TGCT as cancer lineages where PRSS42P 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 PRSS42P — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRSS42P survival associations across molecular data types. PRSS42P RNA expression shows survival associations in the most cancer types (22), 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 PRSS42P RNA expression–survival associations across cancer types. High PRSS42P expression shows unfavorable associations in COAD, but favorable associations in HNSC, KIRP, BRCA, UCS and LAML. The COAD 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 COAD as the clearest survival context for PRSS42P RNA expression.
This table summarizes PRSS42P tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for PRSS42P. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRSS42P shows lower tumor expression in KIRC, KICH and BRCA and higher tumor expression in LUAD, BLCA and LIHC. The KIRC box plot shows higher PRSS42P RNA expression in normal versus tumor tissue (log2 FC = −0.120, t-test p < 0.001).
This table shows molecular features associated with PRSS42P in patient tissues and cancer cell lines. In patient samples, PRSS42P 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, PRSS42P RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
