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BIOMARKER:

IDH2 mutation

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Other names: IDH2, Isocitrate Dehydrogenase (NADP(+)) 2, Isocitrate Dehydrogenase (NADP(+)) 2, Mitochondrial, Isocitrate Dehydrogenase 2 (NADP+), Mitochondrial, Isocitrate Dehydrogenase [NADP], Mitochondrial, Oxalosuccinate Decarboxylase, NADP(+)-Specific ICDH, ICD-M, IDH, IDP, MNADP-IDH, D2HGA2, IDHM, IDPM
Entrez ID:
Related biomarkers:
Related tests:
3d
IDH-mutant adult-type diffuse gliomas: a clinicopathological analysis of 1 301 cases (PubMed, Zhonghua Bing Li Xue Za Zhi)
Compared to supratentorial tumors, non-R132H IDH1 mutations are significantly more frequent in infratentorial tumors. IDH2-mutant gliomas almost exclusively occur in adults and in supratentorial locations, with a significantly higher proportion in oligodendrogliomas than astrocytoma.
Journal
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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IDH1 mutation • IDH2 mutation • IDH1 R132 • IDH2 R172
5d
New P1 trial
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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IDH2 mutation • IDH1 R132 • IDH2 R172
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lomustine • Voranigo (vorasidenib)
6d
Trial primary completion date
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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IDH2 mutation • IDH1 R132 • IDH2 R172
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Voranigo (vorasidenib)
7d
Shared clonal origin of angioimmunoblastic T-cell lymphoma and Burkitt lymphoma arising through divergent evolution from a common precursor. (PubMed, J Hematop)
This case establishes the shared clonal origin between AITL and BL arising in the setting of CH and provides additional biological insight into the development of B-cell lymphoma associated with AITL.
Journal
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IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • DNMT3A (DNA methyltransferase 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • RHOA (Ras homolog family member A) • ID3 (Inhibitor Of DNA Binding 3, HLH Protein)
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IDH2 mutation • TET2 mutation
12d
Omics-based exploration of biomarkers and therapeutic targets in olfactory neuroblastoma. (PubMed, Discov Oncol)
This review consolidates current evidence on candidate biomarkers and therapeutic targets for ONB, highlighting the vital role of omics-based approaches in elucidating its molecular mechanisms. To advance the field, future research should focus on standardizing methods, validating findings in larger, more diverse groups, and integrating multi-omics techniques with AI-driven analyses to enhance diagnostic precision and develop targeted treatments.
Review • Journal
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TP53 (Tumor protein P53) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • HSPA5 (Heat Shock Protein Family A (Hsp70) Member 5) • NEUROD1 (Neuronal Differentiation 1)
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TP53 mutation • IDH2 mutation
14d
Mutant IDH1 blocks neutropoiesis by repressing myeloid progenitor programs. (PubMed, Blood)
This included impaired expression of Cebpe, which encodes a key transcription factor regulating neutrophil differentiation. Reactivation of Cebpe expression, by overexpression of its upstream regulator Cebpa or following treatment with hypomethylating agents restored differentiation, indicating that the differentiation block is reversible.In summary, we found a reversible, pre-leukemic impairment of neutrophil differentiation in IDH1-mutant hematopoiesis that correlates with elevated IDH1 expression in myeloid progenitors and likely explains the strong association of IDH1 mutations with myeloid neoplasms.
Journal
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
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IDH1 mutation • IDH2 mutation
22d
Current landscape and future directions for treatment of accelerated-phase and blast-phase myeloproliferative neoplasms. (PubMed, Semin Hematol)
Given the role of IDH1 and IDH2 mutations in leukemic transformation, targeted therapies with IDH1 or IDH2 inhibitors are another option for selected patients. Current studies are investigating the role of next-generation Janus Kinase (JAK) inhibition, inhibition of epigenetic modulators, and blockade of anti-apoptotic pathways as paradigm shifts to make MPN-AP/BP a more manageable disease.
Journal
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TP53 (Tumor protein P53) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1)
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TP53 mutation • IDH2 mutation • TP53 wild-type
24d
Extended Versus Standard Hypomethylating Agent Dosing in Combination With Venetoclax in Patients With Newly Diagnosed Acute Myeloid Leukemia. (PubMed, Hematol Oncol)
Standard of care (SOC) uses 5-day decitabine (Dec-5) or 7-day azacitidine (Aza-7), while extended HMA regimens (e.g., 10-day decitabine [Dec-10] during cycle 1) have also been explored, although direct comparative data between these approaches are limited. Our findings suggest that Dec-10/Ven may lead to improved transplant rates and survival, providing valuable real-world support for this intensified approach in appropriate patients. Prospective randomized evaluation is warranted.
Clinical • Retrospective data • Journal
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IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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IDH2 mutation
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Venclexta (venetoclax) • azacitidine • decitabine
24d
IDH1 Mutations Are Associated with Favorable Outcomes in Prostate Cancer. (PubMed, Eur Urol)
IDH1 mutations were associated with global transcriptional repression and evidence of metabolic and epigenetic reprogramming. These results depict IDH-mutant prostate cancer as a subtype that can present with high tumor stage and grade, but is associated with favorable outcomes.
Journal
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • RB1 (RB Transcriptional Corepressor 1) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • ERG (ETS Transcription Factor ERG) • SPOP (Speckle Type BTB/POZ Protein) • FOXA1 (Forkhead Box A1) • TMPRSS2 (Transmembrane serine protease 2)
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IDH1 mutation • IDH2 mutation • RB1 mutation • IDH wild-type • IDH1 R132 • TMPRSS2-ERG fusion • IDH2 R172
28d
NCI-2018-00876: Telaglenastat With Radiation Therapy and Temozolomide in Treating Patients With IDH-Mutated Diffuse Astrocytoma or Anaplastic Astrocytoma (clinicaltrials.gov)
P1, N=40, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: May 2026 --> Sep 2026 | Trial primary completion date: May 2026 --> Sep 2026
Trial completion date • Trial primary completion date
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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IDH1 mutation • IDH2 mutation
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temozolomide • telaglenastat (CB-839)
1m
Comprehensive Genomic Profiling of Sinonasal Carcinomas: Identification of Common Mutations and Potential Targets for Therapy. (PubMed, J Neurol Surg B Skull Base)
Treatments include surgery, radiation, and chemotherapy, with ongoing trials investigating agents like cetuximab, cisplatin, and Tazemetostat. Tazemetostat, targeting KMT2D-related DNA (deoxyribonucleic acid) methylation, and cetuximab, targeting the PIK3CA signaling cascade, may offer therapeutic benefits. Further research on mutation-specific therapies could improve treatment strategies.
Journal
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TP53 (Tumor protein P53) • PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • KMT2D (Lysine Methyltransferase 2D) • FAT1 (FAT atypical cadherin 1) • PRKDC (Protein Kinase, DNA-Activated, Catalytic Subunit)
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TP53 mutation • PIK3CA mutation • IDH2 mutation
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Erbitux (cetuximab) • cisplatin • Tazverik (tazemetostat)