Q-omics provides the consensus-scored MISP3 profile across patient tissues and cancer cell-line models. MISP3 expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in STAD. Among the 18 cancer types available for tumor–normal comparison, MISP3 is differentially expressed in 15, with the highest sampling consensus in KIRC. Additionally, MISP3 RNA expression shows 15,280 significant gene co-expression associations, with the highest sampling consensus in ESCA. Together, these results highlight STAD, KIRC, and ESCA as cancer lineages where MISP3 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 MISP3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MISP3 survival associations across molecular data types. MISP3 RNA expression shows survival associations in the most cancer types (21), followed by 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 MISP3 RNA expression–survival associations across cancer types. High MISP3 expression shows unfavorable associations in UCS, LGG, LIHC and ESCA, but favorable associations in STAD and HNSC. The STAD 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 STAD as the clearest survival context for MISP3 RNA expression.
This table summarizes MISP3 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 5. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MISP3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MISP3 shows lower tumor expression in KIRC, KIRP, KICH and HNSC and higher tumor expression in LIHC and BRCA. The KIRC box plot shows higher MISP3 RNA expression in normal versus tumor tissue (log2 FC = −1.761, t-test p < 0.001).
This table shows molecular features associated with MISP3 in patient tissues and cancer cell lines. In patient samples, MISP3 shows the broadest associations at the RNA and protein expression levels, with ESCA recurring as the lineage with the largest associated feature set. In cancer cell lines, MISP3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in SOFT_TISSUE, while CRISPR and shRNA rows add functional-dependency signals in LUNG_SCLC and LARGE_INTESTINE.
