دورية أكاديمية
أعرض في EDS

The AML microenvironment catalyzes a stepwise evolution to gilteritinib resistance.

التفاصيل البيبلوغرافية
العنوان: The AML microenvironment catalyzes a stepwise evolution to gilteritinib resistance.
المؤلفون: Joshi SK; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Department of Physiology & Pharmacology, School of Medicine, Oregon Health & Science University, Portland, OR, USA; Division of Hematology & Medical Oncology, Department of Medicine, Oregon Health & Science University, Portland, OR, USA., Nechiporuk T; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Division of Hematology & Medical Oncology, Department of Medicine, Oregon Health & Science University, Portland, OR, USA., Bottomly D; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Division of Bioinformatics and Computational Biology, Department of Medical Informatics and Clinical Epidemiology, Oregon Health & Science University, Portland, OR, USA., Piehowski PD; Environmental and Molecular Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Reisz JA; Department of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, CO, USA., Pittsenbarger J; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Division of Hematology & Medical Oncology, Department of Medicine, Oregon Health & Science University, Portland, OR, USA., Kaempf A; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Biostatistics Shared Resource, Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA., Gosline SJC; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Wang YT; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Hansen JR; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Gritsenko MA; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Hutchinson C; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Weitz KK; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Moon J; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Cendali F; Department of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, CO, USA., Fillmore TL; Environmental and Molecular Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Tsai CF; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Schepmoes AA; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Shi T; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Arshad OA; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., McDermott JE; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Babur O; Department of Computer Science, University of Massachusetts, Boston, MA, USA., Watanabe-Smith K; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Computational Biology Program, Oregon Health & Science University, Portland, OR, USA., Demir E; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Department of Molecular and Medical Genetics, Oregon Health & Science University, Portland, OR, USA; Computational Biology Program, Oregon Health & Science University, Portland, OR, USA., D'Alessandro A; Department of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, CO, USA., Liu T; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA., Tognon CE; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Division of Hematology & Medical Oncology, Department of Medicine, Oregon Health & Science University, Portland, OR, USA., Tyner JW; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Division of Hematology & Medical Oncology, Department of Medicine, Oregon Health & Science University, Portland, OR, USA; Department of Cell, Development, & Cancer Biology, Oregon Health & Science University, Portland, OR, USA., McWeeney SK; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Division of Bioinformatics and Computational Biology, Department of Medical Informatics and Clinical Epidemiology, Oregon Health & Science University, Portland, OR, USA., Rodland KD; Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA, USA; Department of Cell, Development, & Cancer Biology, Oregon Health & Science University, Portland, OR, USA., Druker BJ; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Division of Hematology & Medical Oncology, Department of Medicine, Oregon Health & Science University, Portland, OR, USA; Department of Cell, Development, & Cancer Biology, Oregon Health & Science University, Portland, OR, USA., Traer E; Knight Cancer Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA; Division of Hematology & Medical Oncology, Department of Medicine, Oregon Health & Science University, Portland, OR, USA; Department of Cell, Development, & Cancer Biology, Oregon Health & Science University, Portland, OR, USA. Electronic address: traere@ohsu.edu.
المصدر: Cancer cell [Cancer Cell] 2021 Jul 12; Vol. 39 (7), pp. 999-1014.e8. Date of Electronic Publication: 2021 Jun 24.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101130617 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1878-3686 (Electronic) Linking ISSN: 15356108 NLM ISO Abbreviation: Cancer Cell Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Cambridge, Mass. : Cell Press, c2002-
مواضيع طبية MeSH: Drug Resistance, Neoplasm* , Tumor Microenvironment*, Aniline Compounds/*pharmacology , Aurora Kinase B/*metabolism , Biomarkers, Tumor/*metabolism , Gene Expression Regulation, Neoplastic/*drug effects , Leukemia, Myeloid, Acute/*drug therapy , Pyrazines/*pharmacology, Aurora Kinase B/genetics ; Biomarkers, Tumor/genetics ; Exome ; Humans ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/pathology ; Metabolome ; Protein Kinase Inhibitors/pharmacology ; Proteome ; Tumor Cells, Cultured
مستخلص: Our study details the stepwise evolution of gilteritinib resistance in FLT3-mutated acute myeloid leukemia (AML). Early resistance is mediated by the bone marrow microenvironment, which protects residual leukemia cells. Over time, leukemia cells evolve intrinsic mechanisms of resistance, or late resistance. We mechanistically define both early and late resistance by integrating whole-exome sequencing, CRISPR-Cas9, metabolomics, proteomics, and pharmacologic approaches. Early resistant cells undergo metabolic reprogramming, grow more slowly, and are dependent upon Aurora kinase B (AURKB). Late resistant cells are characterized by expansion of pre-existing NRAS mutant subclones and continued metabolic reprogramming. Our model closely mirrors the timing and mutations of AML patients treated with gilteritinib. Pharmacological inhibition of AURKB resensitizes both early resistant cell cultures and primary leukemia cells from gilteritinib-treated AML patients. These findings support a combinatorial strategy to target early resistant AML cells with AURKB inhibitors and gilteritinib before the expansion of pre-existing resistance mutations occurs.
Competing Interests: Declaration of interests B.J.D. potential competing interests—SAB: Aileron Therapeutics, Therapy Architects (ALLCRON), Cepheid, Vivid Biosciences, Celgene, RUNX1 Research Program, Novartis, Gilead Sciences (inactive), Monojul (inactive); SAB & Stock: Aptose Biosciences, Blueprint Medicines, EnLiven Therapeutics, Iterion Therapeutics, Third Coast Therapeutics, GRAIL (SAB inactive); Scientific Founder: MolecularMD (inactive, acquired by ICON); Board of Directors & Stock: Amgen, Vincera Pharma; Board of Directors: Burroughs Wellcome Fund, CureOne; Joint Steering Committee: Beat AML LLS; Founder: VB Therapeutics; Sponsored Research Agreement: EnLiven Therapeutics; Clinical Trial Funding: Novartis, Bristol-Myers Squibb, Pfizer; Royalties from Patent 6958335 (Novartis exclusive license) and OHSU and Dana-Farber Cancer Institute (one Merck exclusive license and one CytoImage, Inc., exclusive license). E.T. potential competing interests—Advisory Board/Consulting: Abbvie, Agios, Astellas, Daiichi-Sankyo; Clinical Trial Funding: Janssen, Incyte, LLS BeatAML. Stock options: Notable Labs. J.W.T. potential competing interests—research support: Agios, Aptose, Array, AstraZeneca, Constellation, Genentech, Gilead, Incyte, Janssen, Petra, Seattle Genetics, Syros, Tolero and Takeda. A.D. potential competing interests—founder: Omix Technologies, Inc., and Altis Biosciences, LLC; Consultant: Hemanext Inc. All other authors declare no potential competing interests.
(Copyright © 2021 Elsevier Inc. All rights reserved.)
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معلومات مُعتمدة: U01 CA214116 United States CA NCI NIH HHS; U54 CA224019 United States CA NCI NIH HHS; R50 CA251708 United States CA NCI NIH HHS; P30 CA046934 United States CA NCI NIH HHS; U24 CA210955 United States CA NCI NIH HHS; U24 CA271012 United States CA NCI NIH HHS; U01 CA217862 United States CA NCI NIH HHS; F30 CA239335 United States CA NCI NIH HHS
فهرسة مساهمة: Keywords: AML; Aurora kinase B; FLT3; NRAS; drug resistance; gilteritinib; lipid metabolism; quizartinib; tumor microenvironment; tyrosine kinase inhibitor
المشرفين على المادة: 0 (Aniline Compounds)
0 (Biomarkers, Tumor)
0 (Protein Kinase Inhibitors)
0 (Proteome)
0 (Pyrazines)
0 (gilteritinib)
EC 2.7.11.1 (AURKB protein, human)
EC 2.7.11.1 (Aurora Kinase B)
تواريخ الأحداث: Date Created: 20210625 Date Completed: 20211220 Latest Revision: 20240923
رمز التحديث: 20240923
مُعرف محوري في PubMed: PMC8686208
DOI: 10.1016/j.ccell.2021.06.003
PMID: 34171263
قاعدة البيانات: MEDLINE
الوصف
تدمد:1878-3686
DOI:10.1016/j.ccell.2021.06.003