Q-omics provides the consensus-scored PRR15L profile across patient tissues and cancer cell-line models. PRR15L expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, PRR15L is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, PRR15L RNA expression shows 17,438 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight MESO, KIRC, and TGCT as cancer lineages where PRR15L 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 PRR15L — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PRR15L survival associations across molecular data types. PRR15L RNA expression shows survival associations in the most cancer types (24), followed by mass-spec protein abundance (5). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PRR15L RNA expression–survival associations across cancer types. High PRR15L expression shows unfavorable associations in ACC and ESCA, but favorable associations in MESO, KIRP, STAD and COAD. The MESO 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 MESO as the clearest survival context for PRR15L RNA expression.
This table summarizes PRR15L tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 13, while mass-spec protein shows differences in 3. The strongest signals are observed in KIRC for RNA and COAD for protein.
This table ranks reproducible tumor–normal expression differences for PRR15L. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PRR15L shows lower tumor expression in KIRC, THCA, HNSC, LUSC and KICH and higher tumor expression in BRCA. The KIRC box plot shows higher PRR15L RNA expression in normal versus tumor tissue (log2 FC = −3.996, t-test p < 0.001).
This table shows molecular features associated with PRR15L in patient tissues and cancer cell lines. In patient samples, PRR15L 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, PRR15L RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and BLOOD_Leukemia.
