Q-omics provides the consensus-scored IDH2 profile across patient tissues and cancer cell-line models. IDH2 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, IDH2 is differentially expressed in 11, with the highest sampling consensus in KIRP. Additionally, IDH2 protein abundance shows 19,992 significant protein co-abundance associations, with the highest sampling consensus in HNSC. Together, these results highlight UVM, KIRP, and HNSC as cancer lineages where IDH2 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 IDH2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes IDH2 survival associations across molecular data types. IDH2 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (4) 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 IDH2 RNA expression–survival associations across cancer types. High IDH2 expression shows unfavorable associations in UVM and MESO, but favorable associations in LUSC, SCLC, STAD and GBM. The UVM 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 UVM as the clearest survival context for IDH2 RNA expression.
This table summarizes IDH2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 7. The strongest signals are observed in KIRP for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for IDH2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. IDH2 shows lower tumor expression in KIRP and KIRC and higher tumor expression in LUAD, COAD, BRCA and LUSC. The KIRP box plot shows higher IDH2 RNA expression in normal versus tumor tissue (log2 FC = −1.518, t-test p < 0.001).
This table shows molecular features associated with IDH2 in patient tissues and cancer cell lines. In patient samples, IDH2 shows the broadest associations at the RNA and protein expression levels, with HNSC recurring as the lineage with the largest associated feature set. In cancer cell lines, IDH2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in KIDNEY, while CRISPR and shRNA rows add functional-dependency signals in LUNG_NSCLC_LUAD and BLOOD_Leukemia.
