Q-omics provides the consensus-scored M6PR profile across patient tissues and cancer cell-line models. M6PR expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, M6PR is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, M6PR protein abundance shows 26,298 significant protein co-abundance associations, with the highest sampling consensus in CCRCC. Together, these results highlight MESO, HNSC, and CCRCC as cancer lineages where M6PR 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 M6PR — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes M6PR survival associations across molecular data types. M6PR RNA expression shows survival associations in the most cancer types (20), followed by mutation status (2) and mass-spec protein abundance (9). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible M6PR RNA expression–survival associations across cancer types. High M6PR expression shows unfavorable associations in MESO, COAD, LGG and PAAD, but favorable associations in KIRC and STAD. The MESO Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .003). Together, the overview and detailed table identify MESO as the clearest survival context for M6PR RNA expression.
This table summarizes M6PR tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 8. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for M6PR. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. M6PR shows lower tumor expression in THCA and higher tumor expression in HNSC, COAD, BLCA, KIRP and STAD. The HNSC box plot shows higher M6PR RNA expression in tumor versus normal tissue (log2 FC = +1.013, t-test p < 0.001).
This table shows molecular features associated with M6PR in patient tissues and cancer cell lines. In patient samples, M6PR shows the broadest associations at the RNA and protein expression levels, with CCRCC recurring as the lineage with the largest associated feature set. In cancer cell lines, M6PR 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 STOMACH and BLOOD_Lymphoma.
