Q-omics provides the consensus-scored MSH6 profile across patient tissues and cancer cell-line models. MSH6 expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, MSH6 is differentially expressed in 15, with the highest sampling consensus in HNSC. Additionally, MSH6 protein abundance shows 40,236 significant protein co-abundance associations, with the highest sampling consensus in LSCC. Together, these results highlight MESO, HNSC, and LSCC as cancer lineages where MSH6 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 MSH6 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes MSH6 survival associations across molecular data types. MSH6 RNA expression shows survival associations in the most cancer types (28), followed by mutation status (8) and mass-spec protein abundance (12). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible MSH6 RNA expression–survival associations across cancer types. High MSH6 expression shows unfavorable associations in MESO, KIRP, ACC and LIHC, but favorable associations in KIRC and UCS. The MESO 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 MESO as the clearest survival context for MSH6 RNA expression.
This table summarizes MSH6 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 15, while mass-spec protein shows differences in 12. The strongest signals are observed in HNSC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for MSH6. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. MSH6 shows higher tumor expression in HNSC, COAD, LIHC, BLCA, LUAD and BRCA. The HNSC box plot shows higher MSH6 RNA expression in tumor versus normal tissue (log2 FC = +1.457, t-test p < 0.001).
This table shows molecular features associated with MSH6 in patient tissues and cancer cell lines. In patient samples, MSH6 shows the broadest associations at the RNA and protein expression levels, with LSCC recurring as the lineage with the largest associated feature set. In cancer cell lines, MSH6 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and BLOOD_Lymphoma.
