Q-omics provides the consensus-scored CHRM3 profile across patient tissues and cancer cell-line models. CHRM3 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, CHRM3 is differentially expressed in 14, with the highest sampling consensus in HNSC. Additionally, CHRM3 protein abundance shows 29,774 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight KIRC, HNSC, and LUAD as cancer lineages where CHRM3 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 CHRM3 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes CHRM3 survival associations across molecular data types. CHRM3 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (9) 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 CHRM3 RNA expression–survival associations across cancer types. High CHRM3 expression shows unfavorable associations in UVM, CESC and LGG, but favorable associations in KIRC, SCLC and LUSC. 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 CHRM3 RNA expression.
This table summarizes CHRM3 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 7. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for CHRM3. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. CHRM3 shows lower tumor expression in KIRP, BLCA, KICH and LUAD and higher tumor expression in HNSC and LUSC. The HNSC box plot shows higher CHRM3 RNA expression in tumor versus normal tissue (log2 FC = +1.193, t-test p < 0.001).
This table shows molecular features associated with CHRM3 in patient tissues and cancer cell lines. In patient samples, CHRM3 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, CHRM3 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BONE, while CRISPR and shRNA rows add functional-dependency signals in BREAST and UPPER_AERODIGESTIVE_TRACT.
