Q-omics provides the consensus-scored MIPEP profile across patient tissues and cancer cell-line models. MIPEP expression is associated with patient survival in 22 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, MIPEP is differentially expressed in 14, with the highest sampling consensus in COAD. Additionally, MIPEP protein abundance shows 19,766 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight KIRP, COAD, and LSCC as cancer lineages where MIPEP 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 MIPEP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MIPEP survival associations across molecular data types. MIPEP RNA expression shows survival associations in the most cancer types (22), followed by mutation status (8) 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 MIPEP RNA expression–survival associations across cancer types. High MIPEP expression shows unfavorable associations in LGG and UVM, but favorable associations in KIRP, KIRC, STAD and READ. The KIRP 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 KIRP as the clearest survival context for MIPEP RNA expression.
This table summarizes MIPEP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 6. The strongest signals are observed in COAD for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MIPEP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MIPEP shows lower tumor expression in THCA, KICH, KIRC and HNSC and higher tumor expression in COAD and STAD. The COAD box plot shows higher MIPEP RNA expression in tumor versus normal tissue (log2 FC = +0.958, t-test p < 0.001).
This table shows molecular features associated with MIPEP in patient tissues and cancer cell lines. In patient samples, MIPEP 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, MIPEP 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 BLOOD_Lymphoma and SKIN.
