Q-omics provides the consensus-scored RPAIN profile across patient tissues and cancer cell-line models. RPAIN expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, RPAIN is differentially expressed in 13, with the highest sampling consensus in KIRC. Additionally, RPAIN RNA expression shows 20,643 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KICH, KIRC, and ACC as cancer lineages where RPAIN 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 RPAIN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes RPAIN survival associations across molecular data types. RPAIN RNA expression shows survival associations in the most cancer types (25), followed by mutation status (1) and mass-spec protein abundance (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible RPAIN RNA expression–survival associations across cancer types. High RPAIN expression shows unfavorable associations in KICH, DLBC, ACC and PRAD, but favorable associations in BLCA and PAAD. The KICH 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 KICH as the clearest survival context for RPAIN RNA expression.
This table summarizes RPAIN 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 2. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for RPAIN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. RPAIN shows lower tumor expression in KICH and higher tumor expression in KIRC, COAD, HNSC, BLCA and CHOL. The KIRC box plot shows higher RPAIN RNA expression in tumor versus normal tissue (log2 FC = +0.468, t-test p < 0.001).
This table shows molecular features associated with RPAIN in patient tissues and cancer cell lines. In patient samples, RPAIN shows the broadest associations at the RNA and protein expression levels, with ACC recurring as the lineage with the largest associated feature set. In cancer cell lines, RPAIN 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 KIDNEY and BLOOD_Leukemia.
