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Tytuł pozycji:

Enasidenib-induced differentiation promotes sensitivity to venetoclax in IDH2-mutated acute myeloid leukemia.

Tytuł:
Enasidenib-induced differentiation promotes sensitivity to venetoclax in IDH2-mutated acute myeloid leukemia.
Autorzy:
Cathelin S; Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Sharon D; Oncology Discovery, AbbVie Inc., North Chicago, IL, USA.
Subedi A; Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Cojocari D; Oncology Discovery, AbbVie Inc., North Chicago, IL, USA.
Phillips DC; Oncology Discovery, AbbVie Inc., North Chicago, IL, USA.
Leverson JD; Oncology Development, AbbVie Inc., North Chicago, IL, USA.
MacBeth KJ; Bristol Myers Squibb, Summit, NJ, USA.
Nicolay B; Agios Pharmaceuticals, Inc., Cambridge, MA, USA.
Narayanaswamy R; Agios Pharmaceuticals, Inc., Cambridge, MA, USA.
Ronseaux S; Agios Pharmaceuticals, Inc., Cambridge, MA, USA.
Liu G; Agios Pharmaceuticals, Inc., Cambridge, MA, USA.
Chan SM; Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada. .
Źródło:
Leukemia [Leukemia] 2022 Mar; Vol. 36 (3), pp. 869-872. Date of Electronic Publication: 2021 Nov 06.
Typ publikacji:
Letter
Język:
English
Imprint Name(s):
Publication: 2000- : London : Nature Publishing Group, Specialist Journals
Original Publication: [Baltimore, Md.] : Williams & Wilkins, [c1987-
MeSH Terms:
Aminopyridines/*pharmacology
Antineoplastic Agents/*pharmacology
Bridged Bicyclo Compounds, Heterocyclic/*pharmacology
Enzyme Inhibitors/*pharmacology
Isocitrate Dehydrogenase/*genetics
Leukemia, Myeloid, Acute/*drug therapy
Sulfonamides/*pharmacology
Triazines/*pharmacology
Aminopyridines/therapeutic use ; Animals ; Antineoplastic Agents/therapeutic use ; Bridged Bicyclo Compounds, Heterocyclic/therapeutic use ; Cell Line, Tumor ; Enzyme Inhibitors/therapeutic use ; Humans ; Isocitrate Dehydrogenase/antagonists & inhibitors ; Leukemia, Myeloid, Acute/genetics ; Mutation/drug effects ; Sulfonamides/therapeutic use ; Triazines/therapeutic use
References:
Ward PS, Patel J, Wise DR, Abdel-Wahab O, Bennett BD, Coller HA, et al. The common feature of leukemia-associated IDH1 and IDH2 mutations is a neomorphic enzyme activity converting alpha-ketoglutarate to 2-hydroxyglutarate. Cancer Cell. 2010;17:225–34. (PMID: 10.1016/j.ccr.2010.01.020)
Losman JA, Looper RE, Koivunen P, Lee S, Schneider RK, McMahon C. et al. (R)-2-hydroxyglutarate is sufficient to promoteleukemogenesis and its effects are reversible. Science. 2013;339:1621–5. (PMID: 10.1126/science.1231677)
Gross S, Cairns RA, Minden MD, Driggers EM, Bittinger MA, Jang HG, et al. Cancer-associated metabolite 2-hydroxyglutarate accumulates in acute myelogenous leukemia with isocitrate dehydrogenase 1 and 2 mutations. J Exp Med. 2010;207:339–44. (PMID: 10.1084/jem.20092506)
Yen K, Travins J, Wang F, David MD, Artin E, Straley K. et al. AG-221, a first-in-class therapy targeting acute myeloid leukemia harboring oncogenic IDH2 mutations. Cancer Disco. 2017;7:478–93. (PMID: 10.1158/2159-8290.CD-16-1034)
Amatangelo MD, Quek L, Shih A, Stein EM, Roshal M, David MD, et al. Enasidenib induces acute myeloid leukemia cell differentiation to promote clinical response. Blood. 2017;130:732–41. (PMID: 10.1182/blood-2017-04-779447)
Stein EM, DiNardo CD, Pollyea DA, Fathi AT, Roboz GJ, Altman JK, et al. Enasidenib in mutant IDH2 relapsed or refractory acute myeloid leukemia. Blood. 2017;130:722–31. (PMID: 10.1182/blood-2017-04-779405)
Stein EM, DiNardo CD, Fathi AT, Pollyea DA, Stone RM, Altman JK, et al. Molecular remission and response patterns in patients with mutant-IDH2 acute myeloid leukemia treated with enasidenib. Blood. 2019;133:676–87. (PMID: 10.1182/blood-2018-08-869008)
Chan SM, Thomas D, Corces-Zimmerman MR, Xavy S, Rastogi S, Hong WJ, et al. Isocitrate dehydrogenase 1 and 2 mutations induce BCL-2 dependence in acute myeloid leukemia. Nat Med. 2015;21:178–84. (PMID: 10.1038/nm.3788)
Bisaillon R, Moison C, Thiollier C, Krosl J, Bordeleau ME, Lehnertz B, et al. Genetic characterization of ABT-199 sensitivity in human AML. Leukemia. 2020;34:63–74. (PMID: 10.1038/s41375-019-0485-x)
Konopleva M, Pollyea DA, Potluri J, Chyla B, Hogdal L, Busman T. et al. Efficacy and biological correlates of response in a Phase II study of venetoclax monotherapy in patients with acute myelogenous leukemia. Cancer Disco. 2016;6:1106–17. (PMID: 10.1158/2159-8290.CD-16-0313)
Chyla B, Daver N, Doyle K, McKeegan E, Huang X, Ruvolo V, et al. Genetic biomarkers of sensitivity and resistance to venetoclax monotherapy in patients with relapsed acute myeloid leukemia. Am. J. Hematol. 2018;93:E202–E205.
DiNardo CD, Tiong IS, Quaglieri A, MacRaild S, Loghavi S, Brown FC, et al. Molecular patterns of response and treatment failure after frontline venetoclax combinations in older patients with AML. Blood. 2020;135:791–803. (PMID: 10.1182/blood.2019003988)
Wei AH, Montesinos P, Ivanov V, DiNardo CD, Novak J, Laribi K, et al. Venetoclax plus LDAC for newly diagnosed AML ineligible for intensive chemotherapy: a phase 3 randomized placebo-controlled trial. Blood. 2020;135:2137–45. (PMID: 10.1182/blood.2020004856)
Bradbury DA, Aldington S, Zhu YM, Russell NH. Down-regulation of bcl-2 in AML blasts by all-trans retinoic acid and its relationship to CD34 antigen expression. Br J Haematol. 1996;94:671–5. (PMID: 10.1046/j.1365-2141.1996.d01-1838.x)
Ketley NJ, Allen PD, Kelsey SM, Newland AC. Modulation of idarubicin-induced apoptosis in human acute myeloid leukemia blasts by all-trans retinoic acid, 1,25(OH)2 vitamin D3, and granulocyte-macrophage colony-stimulating factor. Blood. 1997;90:4578–87. (PMID: 10.1182/blood.V90.11.4578)
Benito A, Grillot D, Nuñez G, Fernández-Luna JL. Regulation and function of Bcl-2 during differentiation-induced cell death in HL-60 promyelocytic cells. Am J Pathol. 1995;146:481–90. (PMID: 78567571869853)
Santos-Beneit AM, Mollinedo F. Expression of genes involved in initiation, regulation, and execution of apoptosis in human neutrophils and during neutrophil differentiation of HL-60 cells. J Leukoc Biol. 2000;67:712–24. (PMID: 10.1002/jlb.67.5.712)
Mengubas K, Riordan FA, Hoffbrand AV, Wickremasinghe RG. Co-ordinated downregulation of bcl-2 and bax expression during granulocytic and macrophage-like differentiation of the HL60 promyelocytic leukaemia cell line. FEBS Lett. 1996;394:356–60. (PMID: 10.1016/0014-5793(96)00983-0)
Grillier I, Umiel T, Elstner E, Collins SJ, Koeffler HP. Alterations of differentiation, clonal proliferation, cell cycle progression and bcl-2 expression in RAR alpha-altered sublines of HL-60. Leukemia. 1997;11:393–400. (PMID: 10.1038/sj.leu.2400575)
Otake Y, Sengupta TK, Bandyopadhyay S, Spicer EK, Fernandes DJ. Retinoid-induced apoptosis in HL-60 cells is associated with nucleolin down-regulation and destabilization of Bcl-2 mRNA. Mol Pharmacol. 2005;67:319–26. (PMID: 10.1124/mol.104.006080)
Substance Nomenclature:
0 (Aminopyridines)
0 (Antineoplastic Agents)
0 (Bridged Bicyclo Compounds, Heterocyclic)
0 (Enzyme Inhibitors)
0 (Sulfonamides)
0 (Triazines)
3T1SS4E7AG (enasidenib)
EC 1.1.1.41 (IDH2 protein, human)
EC 1.1.1.41 (Isocitrate Dehydrogenase)
N54AIC43PW (venetoclax)
Entry Date(s):
Date Created: 20211107 Date Completed: 20220311 Latest Revision: 20220812
Update Code:
20240105
DOI:
10.1038/s41375-021-01468-y
PMID:
34743189
Opinia redakcyjna

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