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  1. Article ; Online: AML genomics: introduction.

    Graubert, Timothy

    Seminars in hematology

    2014  Volume 51, Issue 4, Page(s) 249

    MeSH term(s) Genomics ; Humans ; Leukemia, Myeloid, Acute/genetics
    Language English
    Publishing date 2014-10
    Publishing country United States
    Document type Introductory Journal Article
    ZDB-ID 206923-4
    ISSN 1532-8686 ; 0037-1963
    ISSN (online) 1532-8686
    ISSN 0037-1963
    DOI 10.1053/j.seminhematol.2014.08.008
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  2. Article ; Online: Genomics in childhood acute myeloid leukemia comes of age.

    Brunner, Andrew M / Graubert, Timothy A

    Nature medicine

    2018  Volume 24, Issue 1, Page(s) 7–9

    MeSH term(s) Child ; Genomics ; Humans ; Leukemia, Myeloid, Acute ; Mutation
    Language English
    Publishing date 2018-01-19
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/nm.4469
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  3. Article ; Online: A call to action for acute lymphoblastic leukemia.

    Graubert, Timothy A

    The New England journal of medicine

    2014  Volume 371, Issue 11, Page(s) 1064–1066

    MeSH term(s) Animals ; Female ; Humans ; Male ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Protein Kinase Inhibitors/therapeutic use
    Chemical Substances Protein Kinase Inhibitors
    Language English
    Publishing date 2014-09-11
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMe1407477
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  4. Article ; Online: Targeting R-loop-associated ATR response in myelodysplastic syndrome.

    Nguyen, Hai Dang / Zou, Lee / Graubert, Timothy A

    Oncotarget

    2019  Volume 10, Issue 27, Page(s) 2581–2582

    Language English
    Publishing date 2019-04-05
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.26851
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  5. Article ; Online: Therapy-related myelodysplastic syndrome: models and genetics.

    Graubert, Timothy

    Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

    2009  Volume 16, Issue 1 Suppl, Page(s) S45–7

    MeSH term(s) Animals ; Antineoplastic Agents, Alkylating/adverse effects ; Disease Models, Animal ; Drug-Related Side Effects and Adverse Reactions ; Humans ; Myelodysplastic Syndromes/chemically induced ; Myelodysplastic Syndromes/etiology ; Myelodysplastic Syndromes/genetics ; Radiotherapy/adverse effects
    Chemical Substances Antineoplastic Agents, Alkylating
    Language English
    Publishing date 2009-10-24
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1474865-4
    ISSN 1523-6536 ; 1083-8791
    ISSN (online) 1523-6536
    ISSN 1083-8791
    DOI 10.1016/j.bbmt.2009.10.019
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    Zs.A 5082: Show issues Location:
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    Zs.MO 462: Show issues

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  6. Article ; Online: Clonal hematopoiesis and measurable residual disease assessment in acute myeloid leukemia.

    Hasserjian, Robert P / Steensma, David P / Graubert, Timothy A / Ebert, Benjamin L

    Blood

    2020  Volume 135, Issue 20, Page(s) 1729–1738

    Abstract: Current objectives regarding treatment of acute myeloid leukemia (AML) include achieving complete remission (CR) by clinicopathological criteria followed by interrogation for the presence of minimal/measurable residual disease (MRD) by molecular genetic ... ...

    Abstract Current objectives regarding treatment of acute myeloid leukemia (AML) include achieving complete remission (CR) by clinicopathological criteria followed by interrogation for the presence of minimal/measurable residual disease (MRD) by molecular genetic and/or flow cytometric techniques. Although advances in molecular genetic technologies have enabled highly sensitive detection of AML-associated mutations and translocations, determination of MRD is complicated by the fact that many treated patients have persistent clonal hematopoiesis (CH) that may not reflect residual AML. CH detected in AML patients in CR includes true residual or early recurrent AML, myelodysplastic syndrome or CH that is ancestral to the AML, and independent or newly emerging clones of uncertain leukemogenic potential. Although the presence of AML-related mutations has been shown to be a harbinger of relapse in multiple studies, the significance of other types of CH is less well understood. In patients who undergo allogeneic hematopoietic cell transplantation (HCT), post-HCT clones can be donor-derived and in some cases engender a new myeloid neoplasm that is clonally unrelated to the recipient's original AML. In this article, we discuss the spectrum of CH that can be detected in treated AML patients, propose terminology to standardize nomenclature in this setting, and review clinical data and areas of uncertainty among the various types of posttreatment hematopoietic clones.
    MeSH term(s) Clonal Hematopoiesis/physiology ; Diagnostic Techniques and Procedures ; Hematopoietic Stem Cell Transplantation ; Humans ; Leukemia, Myeloid, Acute/blood ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/pathology ; Leukemia, Myeloid, Acute/therapy ; Medical Oncology/methods ; Neoplasm, Residual ; Prognosis ; Remission Induction ; Transplantation Conditioning ; Transplantation, Homologous
    Language English
    Publishing date 2020-03-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2019004770
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    Zs.MO 364: Show issues

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  7. Article: AML1 and Evi1: coconspirators in MDS/AML?

    Graubert, Timothy

    Blood

    2008  Volume 111, Issue 8, Page(s) 3916–3917

    Abstract: In this issue of Blood, Watanabe-Okochi and colleagues use a mouse bone marrow transplantation model to demonstrate that mutant alleles of AML1 (RUNX1) can initiate a myelodysplastic syndrome (MDS) that progresses to acute myelogenous leukemia (AML) in ... ...

    Abstract In this issue of Blood, Watanabe-Okochi and colleagues use a mouse bone marrow transplantation model to demonstrate that mutant alleles of AML1 (RUNX1) can initiate a myelodysplastic syndrome (MDS) that progresses to acute myelogenous leukemia (AML) in association with overexpression of Evi1.
    Language English
    Publishing date 2008-04-23
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2008-01-135376
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  8. Article ; Online: AML genomics for the clinician.

    Graubert, Timothy / Stone, Richard

    Seminars in hematology

    2014  Volume 51, Issue 4, Page(s) 322–329

    Abstract: Acute myeloid leukemia (AML) is a heterogeneous disease, characterized by frequent resistance to available chemotherapeutic agents. The basic therapy for patients with AML has changed little over the past 30 years. Improvements in outcome in recent ... ...

    Abstract Acute myeloid leukemia (AML) is a heterogeneous disease, characterized by frequent resistance to available chemotherapeutic agents. The basic therapy for patients with AML has changed little over the past 30 years. Improvements in outcome in recent decades in younger adult cohorts have generally been ascribed to better supportive care (ie, transfusion and antimicrobial therapy); older adults with AML continue to fare poorly. The explosion of new knowledge regarding the AML genome has yet to be translated into therapeutic benefit, but analysis of specific molecular features in AML samples has enabled the field to more accurately parse out prognosis and assign appropriate therapies (eg, chemotherapy vs allogeneic stem cell transplantation) for groups of patients. Cytogenetic analysis, whether by metaphase or interphase analysis, has been the main tool used to divide patients into varying prognostic subsets, but it has been modified in recent years to include assessment of mutations in a small number of genes. In the past several years, new technologies have provided strategies to interrogate individual cancer genomes in a broad and in-depth fashion. The present article discusses the potential of these new technologies, particularly gene panel and whole-exome or whole-genome sequencing, to improve diagnosis, prognosis, and therapeutic outcome in AML.
    MeSH term(s) Genetic Predisposition to Disease ; Genome, Human ; Genomics ; Humans ; Leukemia, Myeloid, Acute/genetics ; Mutation ; Sequence Analysis, DNA
    Language English
    Publishing date 2014-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 206923-4
    ISSN 1532-8686 ; 0037-1963
    ISSN (online) 1532-8686
    ISSN 0037-1963
    DOI 10.1053/j.seminhematol.2014.08.006
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  9. Article ; Online: Splicing factor gene mutations in hematologic malignancies.

    Saez, Borja / Walter, Matthew J / Graubert, Timothy A

    Blood

    2016  Volume 129, Issue 10, Page(s) 1260–1269

    Abstract: Alternative splicing generates a diversity of messenger RNA (mRNA) transcripts from a single mRNA precursor and contributes to the complexity of our proteome. Splicing is perturbed by a variety of mechanisms in cancer. Recurrent mutations in splicing ... ...

    Abstract Alternative splicing generates a diversity of messenger RNA (mRNA) transcripts from a single mRNA precursor and contributes to the complexity of our proteome. Splicing is perturbed by a variety of mechanisms in cancer. Recurrent mutations in splicing factors have emerged as a hallmark of several hematologic malignancies. Splicing factor mutations tend to occur in the founding clone of myeloid cancers, and these mutations have recently been identified in blood cells from normal, healthy elderly individuals with clonal hematopoiesis who are at increased risk of subsequently developing a hematopoietic malignancy, suggesting that these mutations contribute to disease initiation. Splicing factor mutations change the pattern of splicing in primary patient and mouse hematopoietic cells and alter hematopoietic differentiation and maturation in animal models. Recent developments in this field are reviewed here, with an emphasis on the clinical consequences of splicing factor mutations, mechanistic insights from animal models, and implications for development of novel therapies targeting the precursor mRNA splicing pathway.
    MeSH term(s) Animals ; Hematologic Neoplasms/genetics ; Humans ; Mutation ; RNA Splicing Factors/genetics
    Chemical Substances RNA Splicing Factors
    Language English
    Publishing date 2016-12-09
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2016-10-692400
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  10. Article ; Online: Genetics of myelodysplastic syndromes: new insights.

    Graubert, Timothy / Walter, Matthew J

    Hematology. American Society of Hematology. Education Program

    2011  Volume 2011, Page(s) 543–549

    Abstract: Myelodysplastic syndromes (MDS) are a heterogenous group of hematologic malignancies characterized by clonal expansion of BM myeloid cells with impaired differentiation. The identification of recurrent mutations in MDS samples has led to new insights ... ...

    Abstract Myelodysplastic syndromes (MDS) are a heterogenous group of hematologic malignancies characterized by clonal expansion of BM myeloid cells with impaired differentiation. The identification of recurrent mutations in MDS samples has led to new insights into the pathophysiology of these disorders. Of particular interest is the recent recognition that genes involved in the regulation of histone function (EZH2, ASXL1, and UTX) and DNA methylation (DNMT3A, IDH1/IDH2, and TET2) are recurrently mutated in MDS, providing an important link between genetic and epigenetic alterations in this disease. The mechanism by which these mutated genes contribute to disease pathogenesis is an active area of research, with a current focus on which downstream target genes may be affected. Recent advances from sequencing studies suggest that multiple mutations are required for MDS initiation and progression to acute myeloid leukemia (AML). The past several years have yielded many new insights, but the complete genetic landscape of MDS is not yet known. Moreover, few (if any) of the findings are sufficiently robust to be incorporated into routine clinical practice at this time. Additional studies will be required to understand the prognostic implications of these mutations for treatment response, progression to AML, and survival.
    MeSH term(s) Chromosome Aberrations ; DNA Methylation/genetics ; Haploinsufficiency/genetics ; Humans ; Karyotyping ; Mutation/genetics ; Myelodysplastic Syndromes/genetics
    Language English
    Publishing date 2011
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 1520-4383
    ISSN (online) 1520-4383
    DOI 10.1182/asheducation-2011.1.543
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