Q-omics provides the consensus-scored DUSP9 profile across patient tissues and cancer cell-line models. DUSP9 expression is associated with patient survival in 29 of 34 cancer types, with the highest sampling consensus in KIRC. Among the 18 cancer types available for tumor–normal comparison, DUSP9 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, DUSP9 RNA expression shows 15,207 significant gene co-expression associations, with the highest sampling consensus in TGCT. Together, these results highlight KIRC, and TGCT as cancer lineages where DUSP9 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 DUSP9 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DUSP9 survival associations across molecular data types. DUSP9 RNA expression shows survival associations in the most cancer types (29), followed by mutation status (6) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible DUSP9 RNA expression–survival associations across cancer types. High DUSP9 expression shows unfavorable associations in KIRC, UCEC, COAD, UVM, KIRP and MESO. The KIRC 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 KIRC as the clearest survival context for DUSP9 RNA expression.
This table summarizes DUSP9 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 3. The strongest signals are observed in KIRC for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for DUSP9. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DUSP9 shows lower tumor expression in KIRC, KIRP and KICH and higher tumor expression in HNSC, LIHC and LUAD. The KIRC box plot shows higher DUSP9 RNA expression in normal versus tumor tissue (log2 FC = −5.886, t-test p < 0.001).
This table shows molecular features associated with DUSP9 in patient tissues and cancer cell lines. In patient samples, DUSP9 shows the broadest associations at the RNA and protein expression levels, with TGCT recurring as the lineage with the largest associated feature set. In cancer cell lines, DUSP9 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in URINARY_TRACT, while CRISPR and shRNA rows add functional-dependency signals in BLOOD_Myeloma and BONE.
