Q-omics provides the consensus-scored PRSS30P profile across patient tissues and cancer cell-line models. PRSS30P expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, PRSS30P is differentially expressed in 10, with the highest sampling consensus in KIRC. Additionally, PRSS30P RNA expression shows 13,907 significant gene co-expression associations, with the highest sampling consensus in KIRP. Together, these results highlight KIRP, and KIRC as cancer lineages where PRSS30P 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 PRSS30P — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRSS30P survival associations across molecular data types. PRSS30P RNA expression shows survival associations in the most cancer types (19). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRSS30P RNA expression–survival associations across cancer types. High PRSS30P expression shows unfavorable associations in KIRP, LUAD and MESO, but favorable associations in READ, BLCA and HNSC. The KIRP 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 KIRP as the clearest survival context for PRSS30P RNA expression.
This table summarizes PRSS30P tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for PRSS30P. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRSS30P shows lower tumor expression in UCEC and KICH and higher tumor expression in KIRC, COAD, STAD and BRCA. The KIRC box plot shows higher PRSS30P RNA expression in tumor versus normal tissue (log2 FC = +0.422, t-test p < 0.001).
This table shows molecular features associated with PRSS30P in patient tissues and cancer cell lines. In patient samples, PRSS30P 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, PRSS30P RNA and mutation anchors are most strongly linked to RNA-expression features, especially in STOMACH, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC.
