melanocortin 2 receptor accessory protein 2Genealiases: C6orf117 · bA51G5.2
Q-omics provides the consensus-scored MRAP2 profile across patient tissues and cancer cell-line models. MRAP2 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, MRAP2 is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, MRAP2 RNA expression shows 20,606 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight ACC, KIRC, and LSCC as cancer lineages where MRAP2 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 MRAP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MRAP2 survival associations across molecular data types. MRAP2 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (2). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MRAP2 RNA expression–survival associations across cancer types. High MRAP2 expression shows unfavorable associations in MESO, but favorable associations in ACC, BRCA, LUSC, UCEC and SKCM. The ACC 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 ACC as the clearest survival context for MRAP2 RNA expression.
This table summarizes MRAP2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 1. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for MRAP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MRAP2 shows lower tumor expression in KIRC, KICH, THCA, KIRP and LUAD and higher tumor expression in LIHC. The KIRC box plot shows higher MRAP2 RNA expression in normal versus tumor tissue (log2 FC = −2.736, t-test p < 0.001).
This table shows molecular features associated with MRAP2 in patient tissues and cancer cell lines. In patient samples, MRAP2 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, MRAP2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and SOFT_TISSUE.
