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    GENE:

    IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)

    i
    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
    2d
    Integration of genomic and clinical variables improves the prediction of myelodysplastic syndromes to acute myeloid leukaemia transformation and prognosis. (PubMed, Br J Haematol)
    This work provides the first genomic characterisation of a diagnosed MDS cohort in China and establishes the first risk prediction model for MDS-to-AML transformation, alongside novel prognostic models for OS and PFS. These tools offer improved prognostic prediction and potential guidance for therapeutic strategies in Chinese patients with MDS.
    Journal
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    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • DNMT3A (DNA methyltransferase 1) • NF1 (Neurofibromin 1) • JAK2 (Janus kinase 2) • SF3B1 (Splicing Factor 3b Subunit 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • ETV6 (ETS Variant Transcription Factor 6) • SRSF2 (Serine and arginine rich splicing factor 2) • BCOR (BCL6 Corepressor) • CSF3R (Colony Stimulating Factor 3 Receptor) • STAT3 (Signal Transducer And Activator Of Transcription 3) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • STAG2 (Stromal Antigen 2) • GATA2 (GATA Binding Protein 2) • CALR (Calreticulin)
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    TP53 mutation • SRSF2 mutation • STAT3 mutation
    4d
    The Prognostic Value of Integrating Copy Number Alteration Profiles in NPM1-Mutated Acute Myeloid Leukemia: An Exploratory Study. (PubMed, Appl Clin Genet)
    This exploratory study suggests that combining CNAs and gene mutation profiles may potentially improve the existing prognostic evaluation system for NPM1-mutated AML patients. Confirmation of these results requires additional validation in larger prospective cohorts.
    Journal
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    FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1) • DNMT3A (DNA methyltransferase 1) • TET2 (Tet Methylcytosine Dioxygenase 2)
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    FLT3-ITD mutation • NPM1 mutation
    4d
    Contemporary Precision Stratification and Prognostic Features of Primary Gliomas in a Southern Chinese Population. (PubMed, Research (Wash D C))
    Contemporary glioma cohorts showed prolonged survival outcomes compared to historical cohorts. An association between anatomic localization and molecular subtypes was also established in this Chinese glioma cohort.
    Journal
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    IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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    IDH wild-type
    4d
    Neoantigen-based Personalized DNA Vaccine With Retifanlimab PD-1 Blockade Therapy in Patients With Newly Diagnosed, Unmethylated Glioblastoma (clinicaltrials.gov)
    P1, N=27, Recruiting, Washington University School of Medicine | N=12 --> 27
    Enrollment change
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    IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • MGMT (6-O-methylguanine-DNA methyltransferase)
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    IDH2 mutation • MGMT promoter methylation • IDH wild-type
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    Zynyz (retifanlimab-dlwr) • neoantigen DNA vaccine
    6d
    Tall cell carcinoma with reversed polarity: case report of a rare special type of breast cancer and review of the literature. (PubMed, Discov Oncol)
    This case underscores the importance of integrating histomorphological features, immunohistochemical profiles, and molecular biomarkers to distinguish TCCRP from other triple-negative breast carcinomas. Recognition of this indolent entity is critical for avoiding overtreatment and ensuring appropriate clinical management, given its favorable prognosis compared to conventional triple-negative breast cancers.
    Journal
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    HER-2 (Human epidermal growth factor receptor 2) • PGR (Progesterone receptor) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • TP63 (Tumor protein 63) • GATA3 (GATA binding protein 3)
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    HER-2 expression • IDH2 R172
    6d
    PARP inhibitor resistance in IDH1-mutant cancers due to loss of end protection factors, 53BP1 and REV7. (PubMed, NAR Cancer)
    To overcome this resistance, we found that treatment with the receptor tyrosine kinase inhibitor, cediranib, previously reported to suppress expression of downstream HDR factors, resensitizes 53BP1 and REV7-knockout cells to PARPi treatment. Our findings identify key pathways driving PARPi resistance in IDH1-mutant cancers and highlight potential therapeutic strategies to overcome this resistance.
    Journal • PARP Biomarker
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    IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • TP53BP1 (Tumor Protein P53 Binding Protein 1)
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    IDH1 mutation
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    Recentin (cediranib)
    7d
    ACSL5 Regulates Glucose Metabolism and Chemotherapy Sensitivity in Colorectal Cancer Cells under Glutamine Deficiency. (PubMed, Adv Sci (Weinh))
    Nonetheless, these metabolic increases also generate reactive oxygen species (ROS), inducing DNA damage and significantly enhancing colorectal cancer cell sensitivity to oxaliplatin. The latter provides an explanation as to why colorectal tumors with high ACSL5 expression display preferentially improved patient outcomes from chemotherapy. Collectively, the findings reveal a new pathway for non-genetic chemotherapy resistance mechanisms, deepen the understanding of metabolic reprogramming in tumor cells, and offer potential therapeutic targets for future treatment strategies.
    Journal
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    TP53 (Tumor protein P53) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • MDM2 (E3 ubiquitin protein ligase) • ACSL5 (Acyl-CoA Synthetase Long Chain Family Member 5)
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    oxaliplatin
    9d
    Metabolic and epigenetic dysregulation in IDH1/2-mutant gliomas: A microglial-mediated mechanism of blood-brain barrier disruption. (PubMed, Int Immunopharmacol)
    This review aims to comprehensively examine the association between IDH1/2 mutations and BBB disruption, elucidating how IDH1/2-mutant gliomas alter tumor-associated metabolic and epigenetic pathways, which subsequently influence microglial activation and polarization, contributing to BBB impairment. Furthermore, we propose that microglia-mediated BBB disruption may be one of the underlying mechanisms contributing to complications in IDH1/2-mutant gliomas, such as vasogenic edema and immune-mediated encephalopathy, both of which are closely associated with BBB breakdown.
    Review • Journal
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    IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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    IDH wild-type
    9d
    Targeted triplet therapies incorporating FLT3 or IDH inhibitors: ready for prime time? (PubMed, Hematology Am Soc Hematol Educ Program)
    Triplet therapies combining hypomethylating agents, venetoclax, and targeted inhibitors are emerging as a promising therapy for older patients with AML unfit for intensive chemotherapy...While effective, the need to remain on indefinite therapy for individuals who are not stem cell transplant candidates and dose optimization/de-escalation strategies remain critical concerns. Herein, we aim to review the current treatment landscape of newly diagnosed and relapsed/refractory FLT3- and IDH1/2-mutated AML and the role of triplet regimens in these molecular subgroups.
    Review • Journal
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    FLT3 (Fms-related tyrosine kinase 3) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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    FLT3-ITD mutation • IDH1 mutation
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    Venclexta (venetoclax)
    10d
    Metabolic reprogramming of CAR T cells: a new frontier in cancer immunotherapy. (PubMed, Front Immunol)
    In conclusion, metabolic engineering, leveraging its impact on epigenetic regulation during CAR T cell manufacturing, is crucial for generating potent, persistent, and functionally resilient products. This approach holds immense promise for expanding the curative potential of CAR T cell therapy to a broader range of cancers, particularly challenging solid tumors.
    Review • Journal
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    IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • ACAT1 (Acetyl-CoA Acetyltransferase 1) • IL15 (Interleukin 15) • IL21 (Interleukin 21) • IL7 (Interleukin 7)
    10d
    Frequency and impact of somatic co-occurring mutations on post-transplant outcomes in acute myeloid leukemia: a multicenter registry analysis on behalf of the EBMT ALWP. (PubMed, Bone Marrow Transplant)
    OS was additionally negatively affected when the ten genes were unmutated. Notably, outcomes were excellent for SAR mutations (2-year LFS 76%, OS 84%), indicating allo-HCT in CR1 can overcome their adverse risk at diagnosis.
    Journal
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    TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1) • DNMT3A (DNA methyltransferase 1) • RUNX1 (RUNX Family Transcription Factor 1) • ASXL1 (ASXL Transcriptional Regulator 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • SRSF2 (Serine and arginine rich splicing factor 2)
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    TP53 mutation • FLT3-ITD mutation • NPM1 mutation • RUNX1 mutation • ASXL1 mutation • TET2 mutation • SRSF2 mutation