Q-omics provides the consensus-scored MISP profile across patient tissues and cancer cell-line models. MISP expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in LUAD. Among the 18 cancer types available for tumor–normal comparison, MISP is differentially expressed in 16, with the highest sampling consensus in KIRC. Additionally, MISP protein abundance shows 18,198 significant protein co-abundance associations, with the highest sampling consensus in UCEC. Together, these results highlight LUAD, KIRC, and UCEC as cancer lineages where MISP 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 MISP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MISP survival associations across molecular data types. MISP RNA expression shows survival associations in the most cancer types (24), followed by mutation status (4) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MISP RNA expression–survival associations across cancer types. High MISP expression shows unfavorable associations in LUAD, PAAD, LUSC and KIRC, but favorable associations in ACC and UCS. The LUAD 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 LUAD as the clearest survival context for MISP RNA expression.
This table summarizes MISP tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 16, while mass-spec protein shows differences in 6. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MISP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MISP shows lower tumor expression in KIRC, KICH and LUSC and higher tumor expression in THCA, STAD and HNSC. The KIRC box plot shows higher MISP RNA expression in normal versus tumor tissue (log2 FC = −2.522, t-test p < 0.001).
This table shows molecular features associated with MISP in patient tissues and cancer cell lines. In patient samples, MISP shows the broadest associations at the RNA and protein expression levels, with UCEC recurring as the lineage with the largest associated feature set. In cancer cell lines, MISP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and OVARY.
