Q-omics provides the consensus-scored CNMD profile across patient tissues and cancer cell-line models. CNMD expression is associated with patient survival in 21 of 34 cancer types, with the highest sampling consensus in SCLC. Among the 18 cancer types available for tumor–normal comparison, CNMD is differentially expressed in 9, with the highest sampling consensus in HNSC. Additionally, CNMD RNA expression shows 14,014 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight SCLC, HNSC, and THYM as cancer lineages where CNMD 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 CNMD — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CNMD survival associations across molecular data types. CNMD RNA expression shows survival associations in the most cancer types (21), followed by mutation status (7) and 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 CNMD RNA expression–survival associations across cancer types. High CNMD expression shows unfavorable associations in LGG and MESO, but favorable associations in SCLC, LUAD, READ and LUSC. The SCLC 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 SCLC as the clearest survival context for CNMD RNA expression.
This table summarizes CNMD tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 9, while mass-spec protein shows differences in 3. The strongest signals are observed in HNSC for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for CNMD. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CNMD shows lower tumor expression in HNSC, THCA, BRCA, KICH, COAD and BLCA. The HNSC box plot shows higher CNMD RNA expression in normal versus tumor tissue (log2 FC = −0.725, t-test p < 0.001).
This table shows molecular features associated with CNMD in patient tissues and cancer cell lines. In patient samples, CNMD 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, CNMD RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in LARGE_INTESTINE and BLOOD_Lymphoma.
