Cited by 241Acute Myeloid Leukemia ResearchRetinoids in leukemia and cellular processesEpigenetics and DNA Methylation

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Mutational Cooperativity Linked to Combinatorial Epigenetic Gain of Function in Acute Myeloid Leukemia

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Shih, Alan H., Jiang, Yanwen, Meydan, Cem, Shank, Kaitlyn, Pandey, Suveg, Barreyro, Laura, Antony-Debre, Ileana, Viale, Agnes, Socci, Nicholas, Sun, Yongming, Robertson, Alexander, Cavatore, Magali, de Stanchina, Elisa, Hricik, Todd, Rapaport, Franck, Woods, Brittany, Wei, Chen, Hatlen, Megan, Baljevic, Muhamed, Nimer, Stephen D., Tallman, Martin, Paietta, Elisabeth, Cimmino, Luisa, Aifantis, Iannis, Steidl, Ulrich, Mason, Chris, Melnick, Ari, Levine, Ross L.·2015·Cancer Cell

DOI 10.1016/j.ccell.2015.03.009PMC PMC4518555

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Abstract

Specific combinations of acute myeloid leukemia (AML) disease alleles, including FLT3 and TET2 mutations, confer distinct biologic features and adverse outcome. We generated mice with mutations in Tet2 and Flt3, which resulted in fully penetrant, lethal AML. Multipotent Tet2(-/-);Flt3(ITD) progenitors (LSK CD48(+)CD150(-)) propagate disease in secondary recipients and were refractory to standard AML chemotherapy and FLT3-targeted therapy. Flt3(ITD) mutations and Tet2 loss cooperatively remodeled DNA methylation and gene expression to an extent not seen with either mutant allele alone, including at the Gata2 locus. Re-expression of Gata2 induced differentiation in AML stem cells and attenuated leukemogenesis. TET2 and FLT3 mutations cooperatively induce AML, with a defined leukemia stem cell population characterized by site-specific changes in DNA methylation and gene expression.

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Authors: Shih, A. H., Jiang, Y., Meydan, C., Shank, K., Pandey, S., Barreyro, L., Antony-Debre, I., Viale, A., Socci, N., Sun, Y., Robertson, A., Cavatore, M., de Stanchina, E., Hricik, T., Rapaport, F., Woods, B., Wei, C., Hatlen, M., Baljevic, M., Nimer, S. D., Tallman, M., Paietta, E., Cimmino, L., Aifantis, I., Steidl, U., Mason, C., Melnick, A., & Levine, R. L.
Affiliations: Memorial Sloan Kettering Cancer Center (US)
Weill Cornell Medicine (US)
Albert Einstein College of Medicine (US)
University of Miami (US)
Montefiore Medical Center (US)
Howard Hughes Medical Institute (US)
Cornell University (US)
Corresponding author: Melnick, Ari
Levine, Ross L.
ORCID: Shih, Alan H.
Jiang, Yanwen
Meydan, Cem
Barreyro, Laura
Viale, Agnes
Socci, Nicholas
Sun, Yongming
de Stanchina, Elisa
Woods, Brittany
Wei, Chen
Nimer, Stephen D.
Tallman, Martin
Paietta, Elisabeth
Cimmino, Luisa
Aifantis, Iannis
Steidl, Ulrich
Melnick, Ari
Levine, Ross L.
Venue: Cancer Cell
Publisher: Elsevier BV
Published: 2015-04
Volume: 27
Issue: 4
Pages: 502-515
ISSN: 1535-6108 (ISSN-L)
DOI: 10.1016/j.ccell.2015.03.009
PMC: PMC4518555
OpenAlex: W1977440531
Cited by: 236
References: 50
Citations by year: 2026: 12 · 2025: 15 · 2024: 12 · 2023: 15 · 2022: 18 · 2021: 22 · 2020: 25 · 2019: 23 · 2018: 19 · 2017: 33 · 2016: 31 · 2015: 11
FWCI: 22.62
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 378 d)
Locations: Cancer Cell (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
HAL (submittedVersion, other-oa)
Funders: National Human Genome Research Institute (R01HG006798)
National Cancer Institute (U10CA180820, R01CA166429, CA172636-01, R01CA169784, R01CA173636, U10CA180827, U10CA021115, P30CA008748, P30CA013330, U24CA196172, R01CA166835)
National Institute of Neurological Disorders and Stroke (R01NS076465)
Topics: Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords: acute myeloid leukemia, TET2, FLT3-ITD, DNA methylation, GATA2, leukemia stem cells, leukemogenesis, mouse model, chemoresistance
MeSH terms: Antineoplastic Agents, Cell Differentiation, Cytarabine, DNA-Binding Proteins, Doxorubicin, Mutation, Proto-Oncogene Proteins, Leukemia, Myeloid, Acute, Gene Expression Regulation, Neoplastic, DNA Methylation, Gene Silencing, Epigenesis, Genetic, Dioxygenases, GATA2 Transcription Factor, fms-Like Tyrosine Kinase 3, Haploinsufficiency

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Mutational Cooperativity Linked to Combinatorial Epigenetic Gain of Function in Acute Myeloid Leukemia

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