Q-omics provides the consensus-scored MYZAP profile across patient tissues and cancer cell-line models. MYZAP expression is associated with patient survival in 26 of 34 cancer types, with the highest sampling consensus in OV. Among the 18 cancer types available for tumor–normal comparison, MYZAP is differentially expressed in 16, with the highest sampling consensus in HNSC. Additionally, MYZAP RNA expression shows 17,646 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight OV, HNSC, and UVM as cancer lineages where MYZAP 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 MYZAP — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MYZAP survival associations across molecular data types. MYZAP RNA expression shows survival associations in the most cancer types (26), followed by mutation status (5) 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 MYZAP RNA expression–survival associations across cancer types. High MYZAP expression shows unfavorable associations in OV, LUSC, LGG and CESC, but favorable associations in BLCA and BRCA. The OV 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 OV as the clearest survival context for MYZAP RNA expression.
This table summarizes MYZAP 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 2. The strongest signals are observed in KIRC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for MYZAP. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MYZAP shows lower tumor expression in HNSC, KIRC, LUAD, BLCA, COAD and THCA. The HNSC box plot shows higher MYZAP RNA expression in normal versus tumor tissue (log2 FC = −2.559, t-test p < 0.001).
This table shows molecular features associated with MYZAP in patient tissues and cancer cell lines. In patient samples, MYZAP shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, MYZAP RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Myeloma.