major intrinsic protein of lens fiberGenealiases: AQP0 · CTRCT15 · LIM1 · MIP26 · MP26
Q-omics provides the consensus-scored MIP profile across patient tissues and cancer cell-line models. MIP expression is associated with patient survival in 19 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, MIP is differentially expressed in 12, with the highest sampling consensus in KIRC. Additionally, MIP RNA expression shows 16,206 significant gene co-expression associations, with the highest sampling consensus in ACC. Together, these results highlight KIRC, and ACC as cancer lineages where MIP 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 MIP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MIP survival associations across molecular data types. MIP RNA expression shows survival associations in the most cancer types (19). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MIP RNA expression–survival associations across cancer types. High MIP expression shows unfavorable associations in KIRC and ACC, but favorable associations in STAD, UCEC, KIRP and LIHC. The KIRC 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 KIRC as the clearest survival context for MIP RNA expression.
This table summarizes MIP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12. The strongest signals are observed in KIRC for RNA.
This table ranks reproducible tumor–normal expression differences for MIP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MIP shows lower tumor expression in LIHC and higher tumor expression in KIRC, BLCA, UCEC, COAD and KIRP. The KIRC box plot shows higher MIP RNA expression in tumor versus normal tissue (log2 FC = +0.050, t-test p < 0.001).
This table shows molecular features associated with MIP in patient tissues and cancer cell lines. In patient samples, MIP 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, MIP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in LIVER and BLOOD_Lymphoma.
