Q-omics provides the consensus-scored MPRIP profile across patient tissues and cancer cell-line models. MPRIP expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, MPRIP is differentially expressed in 13, with the highest sampling consensus in LIHC. Additionally, MPRIP protein abundance shows 27,168 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight UVM, LIHC, and LSCC as cancer lineages where MPRIP 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 MPRIP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MPRIP survival associations across molecular data types. MPRIP RNA expression shows survival associations in the most cancer types (24), followed by mutation status (7) and 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 MPRIP RNA expression–survival associations across cancer types. High MPRIP expression shows unfavorable associations in ACC, LUSC and CESC, but favorable associations in UVM, UCS and KIRC. The UVM 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 UVM as the clearest survival context for MPRIP RNA expression.
This table summarizes MPRIP 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 5. The strongest signals are observed in LIHC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MPRIP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MPRIP shows lower tumor expression in KICH, UCEC, LUSC, BRCA and LUAD and higher tumor expression in LIHC. The LIHC box plot shows higher MPRIP RNA expression in tumor versus normal tissue (log2 FC = +1.159, t-test p < 0.001).
This table shows molecular features associated with MPRIP in patient tissues and cancer cell lines. In patient samples, MPRIP 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, MPRIP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SKIN, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Leukemia and BONE.
