Q-omics provides the consensus-scored MYPN profile across patient tissues and cancer cell-line models. MYPN expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, MYPN is differentially expressed in 8, with the highest sampling consensus in COAD. Additionally, MYPN RNA expression shows 13,376 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight HNSC, COAD, and THYM as cancer lineages where MYPN 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 MYPN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MYPN survival associations across molecular data types. MYPN RNA expression shows survival associations in the most cancer types (25), followed by mutation status (7) and mass-spec protein abundance (1). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MYPN RNA expression–survival associations across cancer types. High MYPN expression shows unfavorable associations in HNSC, UVM, LIHC, STAD and SARC, but favorable associations in OV. The HNSC 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 HNSC as the clearest survival context for MYPN RNA expression.
This table summarizes MYPN 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 2. The strongest signals are observed in COAD for RNA and PDAC for protein.
This table ranks reproducible tumor–normal expression differences for MYPN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MYPN shows lower tumor expression in COAD, HNSC and READ and higher tumor expression in LUAD, LIHC and PAAD. The COAD box plot shows higher MYPN RNA expression in normal versus tumor tissue (log2 FC = −0.771, t-test p < 0.001).
This table shows molecular features associated with MYPN in patient tissues and cancer cell lines. In patient samples, MYPN shows the broadest associations at the RNA and protein expression levels, with THYM recurring as the lineage with the largest associated feature set. In cancer cell lines, MYPN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in PANCREAS and BLOOD_Lymphoma.
