Q-omics provides the consensus-scored CHM profile across patient tissues and cancer cell-line models. CHM expression is associated with patient survival in 20 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CHM is differentially expressed in 10, with the highest sampling consensus in HNSC. Additionally, CHM RNA expression shows 20,524 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight KIRC, HNSC, and THYM as cancer lineages where CHM 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 CHM — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CHM survival associations across molecular data types. CHM RNA expression shows survival associations in the most cancer types (20), followed by mutation status (6) 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 CHM RNA expression–survival associations across cancer types. High CHM expression shows unfavorable associations in LIHC, BLCA, UVM and UCEC, but favorable associations in KIRC and SKCM. The KIRC 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 KIRC as the clearest survival context for CHM RNA expression.
This table summarizes CHM tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 10, while mass-spec protein shows differences in 5. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for CHM. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CHM shows lower tumor expression in THCA, UCEC and KICH and higher tumor expression in HNSC, LIHC and CHOL. The HNSC box plot shows higher CHM RNA expression in tumor versus normal tissue (log2 FC = +0.891, t-test p < 0.001).
This table shows molecular features associated with CHM in patient tissues and cancer cell lines. In patient samples, CHM 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, CHM RNA and mutation anchors are most strongly linked to RNA-expression features, especially in PANCREAS, while CRISPR and shRNA rows add functional-dependency signals in KIDNEY and BLOOD_Lymphoma.
