Q-omics provides the consensus-scored DRP2 profile across patient tissues and cancer cell-line models. DRP2 expression is associated with patient survival in 27 of 34 cancer types, with the highest sampling consensus in KIRP. Among the 18 cancer types available for tumor–normal comparison, DRP2 is differentially expressed in 12, with the highest sampling consensus in LUAD. Additionally, DRP2 RNA expression shows 17,644 significant gene co-expression associations, with the highest sampling consensus in LIHC. Together, these results highlight KIRP, LUAD, and LIHC as cancer lineages where DRP2 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 DRP2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes DRP2 survival associations across molecular data types. DRP2 RNA expression shows survival associations in the most cancer types (27), followed by mutation status (8) 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 DRP2 RNA expression–survival associations across cancer types. High DRP2 expression shows unfavorable associations in KIRP, KIRC, ACC, LUAD and LIHC, but favorable associations in UCS. The KIRP 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 KIRP as the clearest survival context for DRP2 RNA expression.
This table summarizes DRP2 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 3. The strongest signals are observed in LUAD for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for DRP2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. DRP2 shows lower tumor expression in UCEC and BLCA and higher tumor expression in LUAD, BRCA, LUSC and HNSC. The LUAD box plot shows higher DRP2 RNA expression in tumor versus normal tissue (log2 FC = +0.458, t-test p < 0.001).
This table shows molecular features associated with DRP2 in patient tissues and cancer cell lines. In patient samples, DRP2 shows the broadest associations at the RNA and protein expression levels, with LIHC recurring as the lineage with the largest associated feature set. In cancer cell lines, DRP2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LIVER, while CRISPR and shRNA rows add functional-dependency signals in BREAST and BLOOD_Leukemia.
