Q-omics provides the consensus-scored DMPK profile across patient tissues and cancer cell-line models. DMPK expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in MESO. Among the 18 cancer types available for tumor–normal comparison, DMPK is differentially expressed in 12, with the highest sampling consensus in BLCA. Additionally, DMPK RNA expression shows 18,079 significant gene co-expression associations, with the highest sampling consensus in THYM. Together, these results highlight MESO, BLCA, and THYM as cancer lineages where DMPK 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 DMPK — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DMPK survival associations across molecular data types. DMPK RNA expression shows survival associations in the most cancer types (24), followed by mutation status (7) and mass-spec protein abundance (6). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DMPK RNA expression–survival associations across cancer types. High DMPK expression shows unfavorable associations in MESO, COAD, LGG and KIRC, but favorable associations in THYM and BLCA. 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 DMPK RNA expression.
This table summarizes DMPK tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 4. The strongest signals are observed in BLCA for RNA and LUAD for protein.
This table ranks reproducible tumor–normal expression differences for DMPK. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DMPK shows lower tumor expression in BLCA, THCA, UCEC and LUSC and higher tumor expression in LIHC and CHOL. The BLCA box plot shows higher DMPK RNA expression in normal versus tumor tissue (log2 FC = −3.104, t-test p < 0.001).
This table shows molecular features associated with DMPK in patient tissues and cancer cell lines. In patient samples, DMPK 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, DMPK 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 BLOOD_Leukemia and SKIN.
