In vivo anti-tumor effect of PARP inhibition in IDH1/2 mutant MDS/AML resistant to targeted inhibitors of mutant IDH1/2
Treatment options for patients with relapsed/refractory acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are scarce. Recurring mutations, such as mutations in isocitrate dehydrogenase-1 and -2 (IDH1/2) are found in subsets of AML and MDS, are therapeutically targeted by mutant enzyme...
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| Published in | Leukemia Vol. 36; no. 5; pp. 1313 - 1323 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.05.2022
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Treatment options for patients with relapsed/refractory acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are scarce. Recurring mutations, such as mutations in isocitrate dehydrogenase-1 and -2 (IDH1/2) are found in subsets of AML and MDS, are therapeutically targeted by mutant enzyme-specific small molecule inhibitors (IDH
m
i). IDH mutations induce diverse metabolic and epigenetic changes that drive malignant transformation. IDH
m
i alone are not curative and resistance commonly develops, underscoring the importance of alternate therapeutic options. We were first to report that IDH1/2 mutations induce a homologous recombination (HR) defect, which confers sensitivity to poly (ADP)-ribose polymerase inhibitors (PARPi). Here, we show that the PARPi olaparib is effective against primary patient-derived IDH1/2-mutant AML/ MDS xeno-grafts (PDXs). Olaparib efficiently reduced overall engraftment and leukemia-initiating cell frequency as evident in serial transplantation assays in IDH1/2-mutant but not -wildtype AML/MDS PDXs. Importantly, we show that olaparib is effective in both IDH
m
i-naïve and -resistant AML PDXs, critical given the high relapse and refractoriness rates to IDH
m
i. Our pre-clinical studies provide a strong rationale for the translation of PARP inhibition to patients with IDH1/2-mutant AML/ MDS, providing an additional line of therapy for patients who do not respond to or relapse after targeted mutant IDH inhibition. |
|---|---|
| AbstractList | Treatment options for patients with relapsed/refractory acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are scarce. Recurring mutations, such as mutations in isocitrate dehydrogenase-1 and -2 (IDH1/2) are found in subsets of AML and MDS, are therapeutically targeted by mutant enzyme-specific small molecule inhibitors (IDHmi). IDH mutations induce diverse metabolic and epigenetic changes that drive malignant transformation. IDHmi alone are not curative and resistance commonly develops, underscoring the importance of alternate therapeutic options. We were first to report that IDH1/2 mutations induce a homologous recombination (HR) defect, which confers sensitivity to poly (ADP)-ribose polymerase inhibitors (PARPi). Here, we show that the PARPi olaparib is effective against primary patient-derived IDH1/2-mutant AML/ MDS xeno-grafts (PDXs). Olaparib efficiently reduced overall engraftment and leukemia-initiating cell frequency as evident in serial transplantation assays in IDH1/2-mutant but not -wildtype AML/MDS PDXs. Importantly, we show that olaparib is effective in both IDHmi-naïve and -resistant AML PDXs, critical given the high relapse and refractoriness rates to IDHmi. Our pre-clinical studies provide a strong rationale for the translation of PARP inhibition to patients with IDH1/2-mutant AML/ MDS, providing an additional line of therapy for patients who do not respond to or relapse after targeted mutant IDH inhibition.Treatment options for patients with relapsed/refractory acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are scarce. Recurring mutations, such as mutations in isocitrate dehydrogenase-1 and -2 (IDH1/2) are found in subsets of AML and MDS, are therapeutically targeted by mutant enzyme-specific small molecule inhibitors (IDHmi). IDH mutations induce diverse metabolic and epigenetic changes that drive malignant transformation. IDHmi alone are not curative and resistance commonly develops, underscoring the importance of alternate therapeutic options. We were first to report that IDH1/2 mutations induce a homologous recombination (HR) defect, which confers sensitivity to poly (ADP)-ribose polymerase inhibitors (PARPi). Here, we show that the PARPi olaparib is effective against primary patient-derived IDH1/2-mutant AML/ MDS xeno-grafts (PDXs). Olaparib efficiently reduced overall engraftment and leukemia-initiating cell frequency as evident in serial transplantation assays in IDH1/2-mutant but not -wildtype AML/MDS PDXs. Importantly, we show that olaparib is effective in both IDHmi-naïve and -resistant AML PDXs, critical given the high relapse and refractoriness rates to IDHmi. Our pre-clinical studies provide a strong rationale for the translation of PARP inhibition to patients with IDH1/2-mutant AML/ MDS, providing an additional line of therapy for patients who do not respond to or relapse after targeted mutant IDH inhibition. Treatment options for patients with relapsed/refractory acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are scarce. Recurring mutations, such as mutations in isocitrate dehydrogenase-1 and -2 (IDH1/2) are found in subsets of AML and MDS, are therapeutically targeted by mutant enzyme-specific small molecule inhibitors (IDH m i). IDH mutations induce diverse metabolic and epigenetic changes that drive malignant transformation. IDH m i alone are not curative and resistance commonly develops, underscoring the importance of alternate therapeutic options. We were first to report that IDH1/2 mutations induce a homologous recombination (HR) defect, which confers sensitivity to poly (ADP)-ribose polymerase inhibitors (PARPi). Here, we show that the PARPi olaparib is effective against primary patient-derived IDH1/2-mutant AML/ MDS xeno-grafts (PDXs). Olaparib efficiently reduced overall engraftment and leukemia-initiating cell frequency as evident in serial transplantation assays in IDH1/2-mutant but not -wildtype AML/MDS PDXs. Importantly, we show that olaparib is effective in both IDH m i-naïve and -resistant AML PDXs, critical given the high relapse and refractoriness rates to IDH m i. Our pre-clinical studies provide a strong rationale for the translation of PARP inhibition to patients with IDH1/2-mutant AML/ MDS, providing an additional line of therapy for patients who do not respond to or relapse after targeted mutant IDH inhibition. Treatment options for patients with relapsed/refractory acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are scarce. Recurring mutations, such as mutations in isocitrate dehydrogenase-1 and -2 (IDH1/2) are found in subsets of AML and MDS, are therapeutically targeted by mutant enzyme-specific small molecule inhibitors (IDH i). IDH mutations induce diverse metabolic and epigenetic changes that drive malignant transformation. IDH i alone are not curative and resistance commonly develops, underscoring the importance of alternate therapeutic options. We were first to report that IDH1/2 mutations induce a homologous recombination (HR) defect, which confers sensitivity to poly (ADP)-ribose polymerase inhibitors (PARPi). Here, we show that the PARPi olaparib is effective against primary patient-derived IDH1/2-mutant AML/ MDS xeno-grafts (PDXs). Olaparib efficiently reduced overall engraftment and leukemia-initiating cell frequency as evident in serial transplantation assays in IDH1/2-mutant but not -wildtype AML/MDS PDXs. Importantly, we show that olaparib is effective in both IDH i-naïve and -resistant AML PDXs, critical given the high relapse and refractoriness rates to IDH i. Our pre-clinical studies provide a strong rationale for the translation of PARP inhibition to patients with IDH1/2-mutant AML/ MDS, providing an additional line of therapy for patients who do not respond to or relapse after targeted mutant IDH inhibition. Treatment options for patients with relapsed/refractory acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are scarce. Recurring mutations, such as mutations in isocitrate dehydrogenase-1 and -2 (IDH1/2) are found in subsets of AML and MDS, are therapeutically targeted by mutant enzyme-specific small molecule inhibitors (IDHmi). IDH mutations induce diverse metabolic and epigenetic changes that drive malignant transformation. IDHmi alone are not curative and resistance commonly develops, underscoring the importance of alternate therapeutic options. We were first to report that IDH1/2 mutations induce a homologous recombination (HR) defect, which confers sensitivity to poly (ADP)-ribose polymerase inhibitors (PARPi). Here, we show that the PARPi olaparib is effective against primary patient-derived IDH1/2-mutant AML/ MDS xeno-grafts (PDXs). Olaparib efficiently reduced overall engraftment and leukemia-initiating cell frequency as evident in serial transplantation assays in IDH1/2-mutant but not -wildtype AML/MDS PDXs. Importantly, we show that olaparib is effective in both IDHmi-naïve and -resistant AML PDXs, critical given the high relapse and refractoriness rates to IDHmi. Our pre-clinical studies provide a strong rationale for the translation of PARP inhibition to patients with IDH1/2-mutant AML/ MDS, providing an additional line of therapy for patients who do not respond to or relapse after targeted mutant IDH inhibition. Treatment options for patients with relapsed/ refractory acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are scarce. Recurring mutations, such as mutations in isocitrate dehydrogenase-1 and −2 (IDH1/2) are found in subsets of AML and MDS, are therapeutically targeted by mutant enzyme-specific small molecule inhibitors (IDH m i). IDH mutations induce diverse metabolic and epigenetic changes that drive malignant transformation. IDH m i alone are not curative and resistance commonly develops, underscoring the importance of alternate therapeutic options. We were first to report that IDH1/2 mutations induce a homologous recombination (HR) defect which confers sensitivity to poly (ADP)-ribose polymerase inhibitors (PARPi). Here, we show that the PARPi olaparib is effective against primary patient-derived IDH1/2-mutant AML/ MDS xeno-grafts (PDXs). Olaparib efficiently reduced overall engraftment and leukemia-initiating cell frequency as evident in serial transplantation assays in IDH1/2-mutant but not -wildtype AML/MDS PDXs. Importantly, we show that olaparib is effective in both IDH m i-naïve and -resistant AML PDXs, critical given the high relapse and refractoriness rates to IDH m i. Our pre-clinical studies provide a strong rationale for the translation of PARP inhibition to patients with IDH1/2-mutant AML/ MDS, providing an additional line of therapy for patients who do not respond to or relapse after targeted mutant IDH inhibition. |
| Author | Chandhok, Namrata S. Prebet, Thomas Song, Yuanbin Liu, Wei Biancon, Giulia Flavell, Richard A. Gao, Yimeng Sundaram, Ranjini Tebaldi, Toma Wang, Xiaman Halene, Stephanie Fu, Xiaoying Mamillapalli, Padmavathi Bindra, Ranjit S. Gbyli, Rana Patel, Amisha Zeidan, Amer M. |
| AuthorAffiliation | 3 Section of Hematology, Department of Internal Medicine, University of Miami, Coral Gables, FL, USA 2 Current affiliation: Department of Hematologic Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, 510062, China 6 Department of Therapeutic Radiology, Yale University, New Haven, CT, 06520, USA 5 Department of Laboratory Medicine, Shenzhen Children’s Hospital, Shenzhen, P. R. of China 4 Department of Hematology, the Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, P. R. of China 7 Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA 10 Yale Stem Cell Center and Yale RNA Center, Yale University School of Medicine, New Haven, CT, 06520, USA 9 Department of Pathology, Yale University, New Haven, CT, 06520, USA 1 Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine, New |
| AuthorAffiliation_xml | – name: 6 Department of Therapeutic Radiology, Yale University, New Haven, CT, 06520, USA – name: 8 Howard Hughes Medical Institute, Yale University, New Haven, Connecticut, USA – name: 10 Yale Stem Cell Center and Yale RNA Center, Yale University School of Medicine, New Haven, CT, 06520, USA – name: 2 Current affiliation: Department of Hematologic Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, 510062, China – name: 3 Section of Hematology, Department of Internal Medicine, University of Miami, Coral Gables, FL, USA – name: 7 Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA – name: 4 Department of Hematology, the Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, P. R. of China – name: 5 Department of Laboratory Medicine, Shenzhen Children’s Hospital, Shenzhen, P. R. of China – name: 9 Department of Pathology, Yale University, New Haven, CT, 06520, USA – name: 1 Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine, New Haven, CT, 06520, USA |
| Author_xml | – sequence: 1 givenname: Rana orcidid: 0000-0001-5524-0739 surname: Gbyli fullname: Gbyli, Rana organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine – sequence: 2 givenname: Yuanbin orcidid: 0000-0001-5580-5998 surname: Song fullname: Song, Yuanbin email: Songyb@sysucc.org.cn organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine, Department of Hematologic Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine – sequence: 3 givenname: Wei surname: Liu fullname: Liu, Wei organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine – sequence: 4 givenname: Yimeng orcidid: 0000-0003-2954-2789 surname: Gao fullname: Gao, Yimeng organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine – sequence: 5 givenname: Giulia surname: Biancon fullname: Biancon, Giulia organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine – sequence: 6 givenname: Namrata S. surname: Chandhok fullname: Chandhok, Namrata S. organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine, Section of Hematology, Department of Internal Medicine, University of Miami, Sylvester Comprehensive Cancer Center – sequence: 7 givenname: Xiaman surname: Wang fullname: Wang, Xiaman organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine, Department of Hematology, the Second Affiliated Hospital of Xi’an Jiaotong University – sequence: 8 givenname: Xiaoying surname: Fu fullname: Fu, Xiaoying organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine, Department of Laboratory Medicine, Shenzhen Children’s Hospital – sequence: 9 givenname: Amisha surname: Patel fullname: Patel, Amisha organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine – sequence: 10 givenname: Ranjini surname: Sundaram fullname: Sundaram, Ranjini organization: Department of Therapeutic Radiology, Yale University – sequence: 11 givenname: Toma orcidid: 0000-0002-0625-1631 surname: Tebaldi fullname: Tebaldi, Toma organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine, Department of Cellular, Computational and Integrative Biology (CIBIO), University of Trento – sequence: 12 givenname: Padmavathi surname: Mamillapalli fullname: Mamillapalli, Padmavathi organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine – sequence: 13 givenname: Amer M. surname: Zeidan fullname: Zeidan, Amer M. organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine – sequence: 14 givenname: Richard A. orcidid: 0000-0003-4461-0778 surname: Flavell fullname: Flavell, Richard A. organization: Department of Immunobiology, Yale University School of Medicine, Howard Hughes Medical Institute, Yale University – sequence: 15 givenname: Thomas orcidid: 0000-0002-6872-625X surname: Prebet fullname: Prebet, Thomas organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine – sequence: 16 givenname: Ranjit S. surname: Bindra fullname: Bindra, Ranjit S. organization: Department of Therapeutic Radiology, Yale University, Department of Pathology, Yale University – sequence: 17 givenname: Stephanie orcidid: 0000-0002-2737-9810 surname: Halene fullname: Halene, Stephanie email: stephanie.halene@yale.edu organization: Section of Hematology, Department of Internal Medicine and Yale Comprehensive Cancer Center, Yale University School of Medicine, Department of Pathology, Yale University, Yale Stem Cell Center and Yale Center for RNA Science and Medicine, Yale University School of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35273342$$D View this record in MEDLINE/PubMed |
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| Copyright | The Author(s), under exclusive licence to Springer Nature Limited 2022 2022. The Author(s), under exclusive licence to Springer Nature Limited. The Author(s), under exclusive licence to Springer Nature Limited 2022. |
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| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceptualization, S.H., R.S.B. and Y.S.; Methodology, S.H., R.G., and Y.S.; Investigation, Y.S., R.G., W.L., Y.G., G.B., X.W., X.F., N.C., R.S., A.P., T.T., and P.M.; Data analysis, Y.S., R.G. and S.H.; Validation, Y.S., R.G., and S.H.; Writing – Original Draft, S.H., R.G., Y.S.; Writing – Review & Editing, S.H., R.S.B., R.G., Y.S.; Funding Acquisition, S.H. and R.S.B.; Resources, R.G., A.P., A.M.Z., R.A.F. and T.P.; Project Administration, S.H. and R.S.B.; Supervision, S.H. and R.S.B. Co-first authors Author contributions |
| ORCID | 0000-0003-4461-0778 0000-0002-0625-1631 0000-0001-5580-5998 0000-0003-2954-2789 0000-0001-5524-0739 0000-0002-2737-9810 0000-0002-6872-625X |
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| PublicationTitle | Leukemia |
| PublicationTitleAbbrev | Leukemia |
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| PublicationYear | 2022 |
| Publisher | Nature Publishing Group UK Nature Publishing Group |
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| References_xml | – reference: XuWYangHLiuYYangYWangPKimSHOncometabolite 2-hydroxyglutarate is a competitive inhibitor of alpha-ketoglutarate-dependent dioxygenasesCancer Cell20111917301:CAS:528:DC%2BC3MXpvValsQ%3D%3D21251613322930410.1016/j.ccr.2010.12.014 – reference: ClarkOYenKMellinghoffIKMolecular pathways: isocitrate dehydrogenase mutations in cancerClin Cancer Res2016221837421:CAS:528:DC%2BC28XmsFeqsrg%3D26819452483426610.1158/1078-0432.CCR-13-1333 – reference: LapidotTSirardCVormoorJMurdochBHoangTCaceres-CortesJA cell initiating human acute myeloid leukaemia after transplantation into SCID miceNature199436764581:STN:280:DyaK2c7ltVKrsg%3D%3D750904410.1038/367645a0 – reference: WinerESStoneRMNovel therapy in Acute myeloid leukemia (AML): moving toward targeted approachesTher Adv Hematol20191020406207198606451:CAS:528:DC%2BB3cXitVanuw%3D%3D31321011662491010.1177/2040620719860645 – reference: RongvauxAWillingerTMartinekJStrowigTGeartySVTeichmannLLDevelopment and function of human innate immune cells in a humanized mouse modelNat Biotechnol201432364721:CAS:528:DC%2BC2cXktlGmur4%3D24633240401758910.1038/nbt.2858 – reference: MolenaarRJRadivoyevitchTNagataYKhurshedMPrzychodzenBMakishimaHIDH1/2 Mutations sensitize acute myeloid leukemia to PARP inhibition and this is reversed by IDH1/2-mutant inhibitorsClin Cancer Res2018241705151:CAS:528:DC%2BC1cXmvVejtL0%3D29339439588473210.1158/1078-0432.CCR-17-2796 – reference: MolenaarRJRadivoyevitchTMaciejewskiJPvan NoordenCJBleekerFEThe driver and passenger effects of isocitrate dehydrogenase 1 and 2 mutations in oncogenesis and survival prolongationBiochim Biophys Acta20141846326411:CAS:528:DC%2BC2cXhsVKnt77K24880135 – reference: HardingJJLoweryMAShihAHSchvartzmanJMHouSFamulareCIsoform switching as a mechanism of acquired resistance to mutant isocitrate dehydrogenase inhibitionCancer Disco20188154071:CAS:528:DC%2BB3cXhtFOms7rM10.1158/2159-8290.CD-18-0877 – reference: AmatangeloMDQuekLShihASteinEMRoshalMDavidMDEnasidenib induces acute myeloid leukemia cell differentiation to promote clinical responseBlood2017130732411:CAS:528:DC%2BC2sXitVSku77F28588019555357810.1182/blood-2017-04-779447 – reference: LiuXGongYIsocitrate dehydrogenase inhibitors in acute myeloid leukemiaBiomark Res201971:CAS:528:DC%2BC1cXisFSgur7J31660152680651010.1186/s40364-019-0173-z – reference: RongvauxATakizawaHStrowigTWillingerTEynonEEFlavellRAHuman hemato-lymphoid system mice: current use and future potential for medicineAnnu Rev Immunol201331635741:CAS:528:DC%2BC3sXnsFClsbY%3D23330956412019110.1146/annurev-immunol-032712-095921 – reference: EllegastJMRauchPJKovtonyukLVMullerRWagnerUSaitoYinv(16) and NPM1mut AMLs engraft human cytokine knock-in miceBlood2016128213041:CAS:528:DC%2BC2sXhtlKlurY%3D27581357508460610.1182/blood-2015-12-689356 – reference: ShihabHAGoughJCooperDNStensonPDBarkerGLEdwardsKJPredicting the functional, molecular, and phenotypic consequences of amino acid substitutions using hidden Markov modelsHum Mutat20133457651:CAS:528:DC%2BC3sXit1aq2303331610.1002/humu.22225 – reference: SaitoYEllegastJMRafieiASongYKullDHeikenwalderMPeripheral blood CD34(+) cells efficiently engraft human cytokine knock-in miceBlood20161281829331:CAS:528:DC%2BC2sXhtlSiu7Y%3D27543436505469610.1182/blood-2015-10-676452 – reference: Benjamin D, Sato T, Cibulskis K, Getz G, Stewart C, Lichtenstein L. Calling somatic SNVs and indels with Mutect2. bioRxiv 2019. https://doi.org/10.1101/861054. – reference: RobinsonJTThorvaldsdottirHWengerAMZehirAMesirovJPVariant review with the integrative genomics viewerCancer Res201777e3141:CAS:528:DC%2BC2sXhslOltbjE29092934567898910.1158/0008-5472.CAN-17-0337 – reference: Sulkowski PL, Corso CD, Robinson ND, Scanlon SE, Purshouse KR, Bai H, et al. 2-Hydroxyglutarate produced by neomorphic IDH mutations suppresses homologous recombination and induces PARP inhibitor sensitivity. 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| Snippet | Treatment options for patients with relapsed/refractory acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are scarce. Recurring mutations, such... Treatment options for patients with relapsed/ refractory acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) are scarce. Recurring mutations, such... |
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| SubjectTerms | 13/100 13/106 13/109 13/21 13/31 13/51 45 45/23 64 64/60 692/699/1541/1990/1673 692/699/1541/1990/283/1897 Acute myeloid leukemia Anticancer properties Cancer Research Critical Care Medicine Enzyme Inhibitors - pharmacology Epigenetics Hematology Homologous recombination Homology Humans Inhibitors Intensive Internal Medicine Isocitrate dehydrogenase Isocitrate Dehydrogenase - genetics Isocitrate Dehydrogenase - metabolism Leukemia Leukemia, Myeloid, Acute - drug therapy Leukemia, Myeloid, Acute - genetics Medicine Medicine & Public Health Mutants Mutation Myelodysplastic syndrome Myelodysplastic syndromes Myelodysplastic Syndromes - drug therapy Myelodysplastic Syndromes - genetics Oncology Patients Poly(ADP-ribose) polymerase Poly(ADP-ribose) Polymerase Inhibitors - pharmacology Poly(ADP-ribose) Polymerase Inhibitors - therapeutic use Recurrence Ribose Thermal resistance Transplantation Tumors Xenografts |
| Title | In vivo anti-tumor effect of PARP inhibition in IDH1/2 mutant MDS/AML resistant to targeted inhibitors of mutant IDH1/2 |
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