Q-omics provides the consensus-scored MPST profile across patient tissues and cancer cell-line models. MPST expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in ACC. Among the 18 cancer types available for tumor–normal comparison, MPST is differentially expressed in 8, with the highest sampling consensus in BRCA. Additionally, MPST protein abundance shows 22,814 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight ACC, BRCA, and LUAD as cancer lineages where MPST 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 MPST — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MPST survival associations across molecular data types. MPST RNA expression shows survival associations in the most cancer types (28), followed by mutation status (7) and mass-spec protein abundance (8). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MPST RNA expression–survival associations across cancer types. High MPST expression shows unfavorable associations in ACC, LUAD, KIRC and LIHC, but favorable associations in UCEC and GBM. The ACC 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 ACC as the clearest survival context for MPST RNA expression.
This table summarizes MPST tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 8, while mass-spec protein shows differences in 8. The strongest signals are observed in BRCA for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for MPST. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MPST shows lower tumor expression in BRCA and KICH and higher tumor expression in THCA, BLCA, LIHC and PRAD. The BRCA box plot shows higher MPST RNA expression in normal versus tumor tissue (log2 FC = −0.333, t-test p < 0.001).
This table shows molecular features associated with MPST in patient tissues and cancer cell lines. In patient samples, MPST shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, MPST RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_SCLC, while CRISPR and shRNA rows add functional-dependency signals in OESOPHAGUS and LARGE_INTESTINE.
