Q-omics provides the consensus-scored MRNIP profile across patient tissues and cancer cell-line models. MRNIP expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in KICH. Among the 18 cancer types available for tumor–normal comparison, MRNIP is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, MRNIP RNA expression shows 20,752 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight KICH, KIRC, and UVM as cancer lineages where MRNIP 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 MRNIP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MRNIP survival associations across molecular data types. MRNIP RNA expression shows survival associations in the most cancer types (28), followed by mutation status (3) and mass-spec protein abundance (4). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MRNIP RNA expression–survival associations across cancer types. High MRNIP expression shows unfavorable associations in KICH, UVM, LIHC, CESC and LGG, but favorable associations in BLCA. The KICH Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .004). Together, the overview and detailed table identify KICH as the clearest survival context for MRNIP RNA expression.
This table summarizes MRNIP 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 4. The strongest signals are observed in KIRC for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for MRNIP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MRNIP shows lower tumor expression in BLCA and KICH and higher tumor expression in KIRC, COAD, LIHC and CHOL. The KIRC box plot shows higher MRNIP RNA expression in tumor versus normal tissue (log2 FC = +0.526, t-test p < 0.001).
This table shows molecular features associated with MRNIP in patient tissues and cancer cell lines. In patient samples, MRNIP shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, MRNIP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in OVARY and BLOOD_Lymphoma.
