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GENE:

IDH1 (Isocitrate dehydrogenase (NADP(+)) 1)

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Other names: HEL-216, HEL-S-26, Epididymis Luminal Protein 216, Isocitrate Dehydrogenase 1 (NADP+), Epididymis Secretory Protein Li 26, IDH1, Isocitrate Dehydrogenase (NADP(+)) 1, Isocitrate Dehydrogenase 1 (NADP+), Soluble
3d
NIRADO: Basket Trial Exploring the Efficacy and Safety of the Combination of Niraparib and Dostarlimab (clinicaltrials.gov)
P2, N=51, Terminated, Gustave Roussy, Cancer Campus, Grand Paris | Trial completion date: Dec 2027 --> Feb 2025 | Suspended --> Terminated; Abandon of the partner, GSK
Trial completion date • Trial termination • Pan tumor • Platinum sensitive
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HER-2 (Human epidermal growth factor receptor 2) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • ARID1A (AT-rich interaction domain 1A) • PBRM1 (Polybromo 1) • CDK12 (Cyclin dependent kinase 12) • CHEK2 (Checkpoint kinase 2) • RAD51 (RAD51 Homolog A) • FANCA (FA Complementation Group A) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • RAD51C (RAD51 paralog C) • RAD51D (RAD51 paralog D) • ARID2 (AT-Rich Interaction Domain 2) • BARD1 (BRCA1 Associated RING Domain 1) • NBN (Nibrin Nijmegen Breakage Syndrome 1 (Nibrin)) • RAD54L (DNA Repair And Recombination Protein RAD54) • DRD (DNA Repair Deficiency)
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HER-2 positive • HER-2 amplification • DDR • CDK12 mutation • CHEK2 mutation • BRIP1 mutation • RAD51C mutation • RAD51D mutation • BARD1 mutation
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Zejula (niraparib) • Jemperli (dostarlimab-gxly)
3d
Unveiling the prognostic and immunological role of IFI44 in glioma. (PubMed, Ann Med)
IFI44 may drive glioma progression through dual mechanisms of immune microenvironment remodeling and promotion of tumor cell aggressiveness, supporting its potential as a prognostic biomarker and therapeutic target. Although preliminary knockdown and overexpression assays were performed, the underlying mechanisms of IFI44-mediated immune regulation and tumor progression require further investigation.
Journal • PD(L)-1 Biomarker • IO biomarker
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PD-L1 (Programmed death ligand 1) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • NOTCH1 (Notch 1) • NF1 (Neurofibromin 1) • PD-1 (Programmed cell death 1) • LAG3 (Lymphocyte Activating 3)
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PD-L1 expression • IDH wild-type
4d
Isocitrate Dehydrogenase-Mutant WHO Grade 4 Astrocytoma with BCOR Alteration: Case Report. (PubMed, Case Rep Oncol)
This case represents the first report of a BCOR ITD in an IDH-mutant WHO grade 4 astrocytoma. The discovery expands the molecular spectrum of high-grade astrocytomas and highlights the need for further research into the biological, prognostic, and therapeutic significance of BCOR alterations in these tumors.
Journal
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EGFR (Epidermal growth factor receptor) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • ATRX (ATRX Chromatin Remodeler) • BCOR (BCL6 Corepressor)
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EGFR mutation • IDH1 mutation
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TruSight Oncology 500 Assay
4d
The Value of Detecting and Monitoring ctDNA in Uveal Melanoma: Results of a Pilot Study and a Systematic Review. (PubMed, Case Rep Ophthalmol)
Co-occurrence of GNAQ, GNAS, and IDH1 mutations may represent a molecular signature of recurrence. Further validation in larger cohorts is needed to define optimal gene panels and VAF thresholds for clinical use.
Journal • Circulating tumor DNA
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EGFR (Epidermal growth factor receptor) • FGFR2 (Fibroblast growth factor receptor 2) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • STK11 (Serine/threonine kinase 11) • GNAQ (G Protein Subunit Alpha Q) • BAP1 (BRCA1 Associated Protein 1) • GNAS (GNAS Complex Locus)
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IDH1 mutation
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Ion AmpliSeq™ Cancer Hotspot Panel v2
7d
Integrated Genomic and Transcriptomic Profiling of Isolated Trisomies in AML Reveals Cell Cycle Dysregulation and Therapeutic Vulnerabilities. (PubMed, J Cell Mol Med)
Drug sensitivity profiling revealed subgroup-specific vulnerabilities: IT-8 to DNA damage checkpoint inhibitors, IT-21 to PLK/mTOR inhibitors and IT-13+22 to BRAF/EGFR-targeted agents. These findings highlight AML-IT heterogeneity and therapeutic potential.
Journal
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BRAF (B-raf proto-oncogene) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • DNMT3A (DNA methyltransferase 1) • ASXL1 (ASXL Transcriptional Regulator 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • CALR (Calreticulin) • HSPA5 (Heat Shock Protein Family A (Hsp70) Member 5) • MCM4 (Minichromosome Maintenance Complex Component 4) • CDC25A (Cell Division Cycle 25A) • CDC7 (Cell Division Cycle 7) • GNRP (Ras-Specific Guanine Nucleotide-Releasing Factor 1) • HSP90AB1 (Heat Shock Protein 90 Alpha Family Class B Member 1)
7d
Oncogenic role of IDH1 RNA-binding activity in glioblastoma progression. (PubMed, Biochem Biophys Res Commun)
Using enhanced crosslinking and immunoprecipitation (eCLIP) and RNA immunoprecipitation (RIP), we identified numerous IDH1-bound transcripts, including p62/SQSTM1 which was validated as a functional target. These findings indicate that IDH1 facilitates glioma progression by binding and suppression of p62.
Journal
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • SQSTM1 (Sequestosome 1)
8d
Drug Repurposing for AML: Structure-Based Virtual Screening and Molecular Simulations of FDA-Approved Compounds with Polypharmacological Potential. (PubMed, Biomedicines)
While targeted agents-such as LSD1 inhibitors, the BCL-2 inhibitor venetoclax, and IDH1 inhibitors-have provided clinical benefit, their efficacy is often limited by compensatory signaling and clonal evolution. This computational study supports the feasibility of a polypharmacology-based strategy for AML therapy by integrating epigenetic modulation, apoptotic reactivation, and metabolic correction within single molecular scaffolds. However, the identified compounds (Belumosudil, DB08512, and Elraglusib) have not yet demonstrated efficacy in AML models; further preclinical validation is warranted to substantiate these predictions and advance translational development.
FDA event • Journal • IO biomarker
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1)
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IDH1 mutation • IDH1 R132
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Venclexta (venetoclax) • elraglusib (9-ING-41)
8d
Loss of IDH1 and IDH2 mutations during the evolution of metastatic chondrosarcoma. (PubMed, Genome Biol)
This may reflect either relaxed positive selection for the mutant IDH1 locus, or negative selection for the hypermethylation phenotype later in tumor evolution. This finding highlights the challenge for therapeutic intervention by mutant IDH1 inhibitors in chondrosarcoma.
Journal
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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IDH1 mutation • IDH2 mutation
9d
Chemotherapy Strategies and Their Efficacy for Mesenchymal Chondrosarcoma. (PubMed, Curr Oncol)
Trabectedin demonstrates low disease control rate in translocation-related sarcomas, including few MCS cases. Anti-angiogenic tyrosine kinase inhibitors, such as apatinib and pazopanib, demonstrate activity in chondrosarcoma, but MCS-specific data are lacking. IDH1 inhibition benefits conventional subtypes rather than MCS. Early immunotherapy experience is limited, but pathway-directed strategies targeting BCL2 and PI3K-mTOR warrant evaluation.
Review • Journal
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • BCL2 (B-cell CLL/lymphoma 2) • HEY1 (Hes Related Family BHLH Transcription Factor With YRPW Motif 1) • NCOA2 (Nuclear Receptor Coactivator 2)
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AiTan (rivoceranib) • pazopanib • Yondelis (trabectedin)
9d
Reprogramming the Immune Suppressive Tumor Microenvironment in Glioma Enhances the Efficacy of Immune-Mediated Gene Therapy. (PubMed, bioRxiv)
However, when combined with immune-stimulatory Ad-TK (adenoviral vectors encoding herpes simplex virus thymidine kinase) and Ad-Flt3L (adenoviral vectors encoding FMS-like tyrosine kinase 3 ligand) gene therapy, CD73 blockade significantly enhanced therapeutic efficacy and increased anti-glioma effector T cell activity. These findings reveal that CD73 inhibition used in combination with immune stimulatory Ad-TK/Ad-Flt3L gene therapy may be an effective treatment for wtIDH1 gliomas, which could be readily translated to the clinical arena.
Journal • IO biomarker
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FLT3 (Fms-related tyrosine kinase 3) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • CD73 (5'-Nucleotidase Ecto) • NT5E (5'-Nucleotidase Ecto)
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IDH1 mutation • IDH1 R132
9d
Integrated pathway analysis identifies prognostically relevant subtypes of glioblastoma characterized by abnormalities in multi-omics. (PubMed, Clin Transl Med)
We report the interaction between tumor cells and environmental immune cells, classifying GBM into two main subtypes: 1) The tumor-driving subtype is characterized by multiple oncogenic mutations, while 2) the immune-blockage subtype is marked by a high presence of immune cells. We used integrated multidimensional analyses of somatic mutations, DNA methylation, and RNA transcripts to gain a deeper understanding of GBM biology and potential therapeutic implications.
Journal • PD(L)-1 Biomarker • IO biomarker
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EGFR (Epidermal growth factor receptor) • TP53 (Tumor protein P53) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IFNG (Interferon, gamma)
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TP53 mutation • EGFR mutation • IDH1 mutation