170 results match your criteria amkl gata1

Clinical impact of genomic characterization of 15 patients with acute megakaryoblastic leukemia-related malignancies.

Cold Spring Harb Mol Case Stud 2021 Apr 8;7(2). Epub 2021 Apr 8.

Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA.

Acute megakaryoblastic leukemia (AMKL) is a rare subtype of acute myeloid leukemia but is approximately 500 times more likely to develop in children with Down syndrome (DS) through transformation of transient abnormal myelopoiesis (TAM). This study investigates the clinical significance of genomic heterogeneity of AMKL in children with and without DS and in children with TAM. Genomic evaluation of nine patients with DS-related TAM or AMKL, and six patients with non-DS AMKL, included conventional cytogenetics and a comprehensive next-generation sequencing panel for single-nucleotide variants/indels and copy-number variants in 118 genes and fusions involving 110 genes. Read More

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[Analysis of Clinical Characteristics and Prognosis in Children with Acute Megakaryoblastic Leukemia without Down Syndrome].

Zhongguo Shi Yan Xue Ye Xue Za Zhi 2021 Apr;29(2):374-380

Department of Pediatrics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, Guangdong Province,

Objective: To analyze the clinical characteristics and treatment effects of children with acute megakaryoblastic leukemia without down syndrome (non-DS-AMKL).

Methods: The clinical data of 19 children with non-DS-AMKL treated in the Pediatric Hematology Ward in Sun Yat-sen Memorial Hospital of Sun Yat-sen University from May 2008 to April 2018 were analyzed retrospectively. The clinical characteristics, laboratory test and treatment methods of the children were concluded. Read More

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Acute megakaryoblastic leukemia with a novel GATA1 mutation in a second trimester stillborn fetus with trisomy 21.

Leuk Lymphoma 2021 Mar 30:1-4. Epub 2021 Mar 30.

Unit of Anatomic Pathology, Department of Molecular Medicine, IRCCS San Matteo Foundation, University of Pavia, Pavia, Italy.

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Pluripotent stem cell model of early hematopoiesis in Down syndrome reveals quantitative effects of short-form GATA1 protein on lineage specification.

PLoS One 2021 29;16(3):e0247595. Epub 2021 Mar 29.

Department of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.

Children with Down syndrome (DS) are susceptible to two blood disorders, transient abnormal myelopoiesis (TAM) and Down syndrome-associated acute megakaryocytic leukemia (DS-AMKL). Mutations in GATA binding protein 1 (GATA1) have been identified as the cause of these diseases, and the expression levels of the resulting protein, short-form GATA1 (GATA1s), are known to correlate with the severity of TAM. On the other hand, despite the presence of GATA1 mutations in almost all cases of DS-AMKL, the incidence of DS-AMKL in TAM patients is inversely correlated with the expression of GATA1s. Read More

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Molecular Mechanisms of the Genetic Predisposition to Acute Megakaryoblastic Leukemia in Infants With Down Syndrome.

Front Oncol 2021 11;11:636633. Epub 2021 Mar 11.

Pediatric Hematology and Oncology, Martin Luther University Halle-Wittenberg, Halle, Germany.

Individuals with Down syndrome are genetically predisposed to developing acute megakaryoblastic leukemia. This myeloid leukemia associated with Down syndrome (ML-DS) demonstrates a model of step-wise leukemogenesis with perturbed hematopoiesis already presenting , facilitating the acquisition of additional driver mutations such as truncating variants, which are pathognomonic to the disease. Consequently, the affected individuals suffer from a transient abnormal myelopoiesis (TAM)-a pre-leukemic state preceding the progression to ML-DS. Read More

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[Treatment strategy for myeloid leukemia with Down syndrome].

Takashi Taga

Rinsho Ketsueki 2020 ;61(9):1382-1387

Department of Pediatrics, Shiga University of Medical Science.

Myeloid leukemia with Down syndrome (ML-DS) demonstrates unique characteristics such as the predominance of FAB M7, an age predilection during the first 4 years of life, and higher sensitivity to chemotherapeutic agents, which translate into a good treatment response as well as increased treatment-related toxicities. Consequently, patients with ML-DS have traditionally been treated separately from non-DS acute myeloid leukemia (AML) children. The 3-year event-free survival rates in recent clinical studies in the Western countries and Japan are all more than 85%. Read More

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January 2021

Transient Myeloproliferative Disorder: A Cytogenomic Update.

J Assoc Genet Technol 2020 ;46(2):74-91

The International Circle of Genetic Studies, Los Angeles, CA.

Objectives: Transient myeloproliferative disorder (TMD), now more commonly known as transient abnormal myelopoiesis (TAM), is a condition closely associated with Down syndrome. Ninety-five percent of Down syndrome cases occur as a result of chromosomal nondisjunction and are rarely due to mosaicism or translocation. TMD is found exclusively in neonates and is most commonly characterized by trisomy 21, somatic GATA1 mutation, and the increased presence of megakaryoblasts. Read More

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January 2020

Transient Abnormal Myelopoeisis and Mosaic Down Syndrome in a Phenotypically Normal Newborn.

Children (Basel) 2020 May 28;7(6). Epub 2020 May 28.

Department of Hematology-Oncology, Texas Children's Hospital, Houston, TX 77030, USA.

Transient abnormal myelopoiesis (TAM) is a common and potentially fatal neonatal complication of newborn babies with Down syndrome (DS). Children born with mosaic DS are also at risk of developing TAM. However, due to their variable phenotypes, early identification of patients with mosaic DS may be difficult; thus, early diagnosis of TAM is just as challenging. Read More

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GATA1 and cooperating mutations in myeloid leukaemia of Down syndrome.

IUBMB Life 2020 01 26;72(1):119-130. Epub 2019 Nov 26.

MRC Weatherall Institute of Molecular Medicine, University of Oxford, United Kingdom of Great Britain and Northern Ireland.

Myeloid leukaemia of Down syndrome (ML-DS) is an acute megakaryoblastic/erythroid leukaemia uniquely found in children with Down syndrome (constitutive trisomy 21). It has a unique clinical course, being preceded by a pre-leukaemic condition known as transient abnormal myelopoiesis (TAM), and provides an excellent model to study multistep leukaemogenesis. Both TAM and ML-DS blasts carry acquired N-terminal truncating mutations in the erythro-megakaryocytic transcription factor GATA1. Read More

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January 2020

Ontogenic Changes in Hematopoietic Hierarchy Determine Pediatric Specificity and Disease Phenotype in Fusion Oncogene-Driven Myeloid Leukemia.

Cancer Discov 2019 12 29;9(12):1736-1753. Epub 2019 Oct 29.

INSERM U1170, Gustave Roussy, Villejuif, France.

Fusion oncogenes are prevalent in several pediatric cancers, yet little is known about the specific associations between age and phenotype. We observed that fusion oncogenes, such as , are associated with acute megakaryoblastic or other myeloid leukemia subtypes in an age-dependent manner. Analysis of a novel inducible transgenic mouse model showed that expression in fetal hematopoietic stem cells induced rapid megakaryoblastic leukemia whereas expression in adult bone marrow hematopoietic stem cells resulted in a shift toward myeloid transformation with a strikingly delayed leukemogenic potential. Read More

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December 2019

Highly sensitive detection of GATA1 mutations in patients with myeloid leukemia associated with Down syndrome by combining Sanger and targeted next generation sequencing.

Genes Chromosomes Cancer 2020 03 21;59(3):160-167. Epub 2019 Oct 21.

Department of Pediatrics, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.

Myeloid leukemia associated with Down syndrome (ML-DS) is characterized by a predominance of acute megakaryoblastic leukemia, the presence of GATA1 mutations and a favorable outcome. Because DS children can also develop conventional acute myeloid leukemia with unfavorable outcome, detection of GATA1 mutations is important for diagnosis of ML-DS. However, myelofibrosis and the significant frequency of dry taps have hampered practical screening of GATA1 mutations using bone marrow (BM) samples. Read More

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Acute Megakaryocytic Leukemia.

Cold Spring Harb Perspect Med 2020 02 3;10(2). Epub 2020 Feb 3.

Northwestern University, Division of Hematology/Oncology, Chicago, Illinois 60611, USA.

Acute megakaryoblastic leukemia (AMKL) is a rare malignancy affecting megakaryocytes, platelet-producing cells that reside in the bone marrow. Children with Down syndrome (DS) are particularly prone to developing the disease and have a different age of onset, distinct genetic mutations, and better prognosis as compared with individuals without DS who develop the disease. Here, we discuss the contributions of chromosome 21 genes and other genetic mutations to AMKL, the clinical features of the disease, and the differing features of DS- and non-DS-AMKL. Read More

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February 2020

Megakaryocyte polyploidization: role in platelet production.

Platelets 2020 Aug 22;31(6):707-716. Epub 2019 Sep 22.

UMR 1170, Institut National de la Santé et de la Recherche Médicale, Univ. Paris-Sud, Université Paris-Saclay, Gustave Roussy Cancer Campus, Equipe Labellisée Ligue Nationale Contre le Cancer , Villejuif, France.

Mammal megakaryocytes (MK) undergo polyploidization during their differentiation. This process leads to a marked increase in the MK size and of their cytoplasm. Contrary to division by classical mitosis, ploidization allows an economical manner to produce platelets as they arise from the fragmentation of the MK cytoplasm. Read More

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Pathologic Features of Down Syndrome Myelodysplastic Syndrome and Acute Myeloid Leukemia: A Report From the Children's Oncology Group Protocol AAML0431.

Arch Pathol Lab Med 2020 04 20;144(4):466-472. Epub 2019 Aug 20.

From the Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee (Drs Mast, Mosse, Jones, and Head); the Division of Hematology/Oncology, Children's Hospital of Michigan, Wayne State University, Detroit (Dr Taub); the Department of Biostatistics, University of Southern California, Monrovia (Dr Alonzo and Mr Wang); the Division of Hematology/Oncology/Bone Marrow Transplantation, Children's Mercy Hospital, Kansas City, Missouri (Dr Gamis); the Pathology and Laboratory Medicine Service, VA Tennessee Valley Healthcare System, Nashville (Dr Mosse); the Department of Pediatrics, University of New Mexico, Albuquerque (Dr Mathew); the Division of Hematology-Oncology, IWK Health Centre, Halifax, Nova Scotia, Canada (Dr Berman); the Departments of Oncology (Dr Campana and Ms Coustan-Smith) and Pathology (Dr Raimondi), St. Jude Children's Research Hospital, Memphis, Tennessee; the Department of Pediatrics, Yong Loo Lin School of Medicine, National University of Singapore, The National University Cancer Institute, NUH Medical Centre, Singapore (Dr Campana and Ms Coustan-Smith); the Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis (Dr Hirsch); the Department of Pediatrics, University of Toronto, Toronto, Ontario, Canada (Dr Hitzler); and the Division of Hematology/Oncology, The Hospital for Sick Children Developmental and Stem Cell Biology, The Hospital for Sick Children Research Institute, Toronto, Ontario, Canada (Dr Hitzler). Dr Mast now has a joint appointment at the Pathology and Laboratory Medicine Service, VA Tennessee Valley Healthcare System, Nashville. Dr Mathew is currently at the Department of Pediatrics, Presbyterian Health Services, Albuquerque, New Mexico. Dr Berman is currently at the Department of Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada. Dr Jones is currently at Pathgroup Labs, Nashville, Tennessee. Dr Campana is no longer at the Department of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee. Ms Coustan-Smith is no longer at the Department of Oncology, St. Jude Children's Research Hospital, Memphis, Tennessee.

Context.—: Detailed diagnostic features of acute myeloid leukemia in Down syndrome are lacking, leading to potential misdiagnoses as standard acute myeloid leukemia occurring in patients with Down syndrome.

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Molecular features, prognosis, and novel treatment options for pediatric acute megakaryoblastic leukemia.

Expert Rev Hematol 2019 05 27;12(5):285-293. Epub 2019 Apr 27.

a Department of Hematology , Juntendo University Graduate School of Medicine , Tokyo , Japan.

Introduction: Acute megakaryoblastic leukemia (AMegL) is a rare hematological neoplasm most often diagnosed in children and is commonly associated with Down's syndrome (DS). Although AMegLs are specifically characterized and typically diagnosed by megakaryoblastic expansion, recent advancements in molecular analysis have highlighted the heterogeneity of this disease, with specific cytogenic and genetic alterations characterizing different disease subtypes. Areas covered: This review will focus on describing recurrent molecular variations in both DS and non-DS pediatric AMegL, their role in promoting leukemogenesis, their association with different clinical aspects and prognosis, and finally, their influence on future treatment strategies with a number of specific drugs beyond conventional chemotherapy already under development. Read More

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Triplications of human chromosome 21 orthologous regions in mice result in expansion of megakaryocyte-erythroid progenitors and reduction of granulocyte-macrophage progenitors.

Oncotarget 2018 Jan 19;9(4):4773-4786. Epub 2017 Dec 19.

The Children's Guild Foundation Down Syndrome Research Program, Genetics and Genomics Program and Department of Cancer Genetics and Genomics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

Individuals with Down syndrome (DS) frequently have hematopoietic abnormalities, including transient myeloproliferative disorder and acute megakaryoblastic leukemia which are often accompanied by acquired GATA1 mutations that produce a truncated protein, GATA1s. The mouse has been used for modeling DS based on the syntenic conservation between human chromosome 21 (Hsa21) and three regions in the mouse genome located on mouse chromosome 10 (Mmu10), Mmu16 and Mmu17. To assess the impact of the dosage increase of Hsa21 gene orthologs on the hematopoietic system, we characterized the related phenotype in the model which carries duplications spanning the entire Hsa21 orthologous regions on Mmu10, Mmu16 and Mmu17, and the /+;/+;; model which carries a mutation we engineered. Read More

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January 2018

GATA1 insufficiencies in primary myelofibrosis and other hematopoietic disorders: consequences for therapy.

Expert Rev Hematol 2018 03 19;11(3):169-184. Epub 2018 Feb 19.

d Department of Biomedical and Neuromotorial Sciences , Alma Mater University , Bologna , Italy.

Introduction: GATA1, the founding member of a family of transcription factors, plays important roles in the development of hematopoietic cells of several lineages. Although loss of GATA1 has been known to impair hematopoiesis in animal models for nearly 25 years, the link between GATA1 defects and human blood diseases has only recently been realized. Areas covered: Here the current understanding of the functions of GATA1 in normal hematopoiesis and how it is altered in disease is reviewed. Read More

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GATA1 Is a Sensitive and Specific Nuclear Marker for Erythroid and Megakaryocytic Lineages.

Am J Clin Pathol 2017 Apr;147(4):420-426

From the Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.

Objectives: GATA binding factor 1 (GATA1) is a transcription factor essential for erythromegakaryocytic differentiation. Given its function in lineage specification, we sought to evaluate the immunohistochemical profile of GATA1 in normal marrow and acute leukemia and assess the use of GATA1 as a specific erythromegakaryocytic immunohistochemical marker.

Methods: Immunohistochemical studies for GATA1 expression were performed on bone marrow biopsy specimens to define its role in the evaluation of acute leukemia and other hematologic disorders. Read More

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ETO2-GLIS2 Hijacks Transcriptional Complexes to Drive Cellular Identity and Self-Renewal in Pediatric Acute Megakaryoblastic Leukemia.

Cancer Cell 2017 03;31(3):452-465

INSERM U1170, Equipe Labellisée Ligue Contre le Cancer, Gustave Roussy Institute, 39 rue Camille Desmoulins, 94800 Villejuif, France; Gustave Roussy, 94800 Villejuif, France; Université Paris Diderot, 75013 Paris, France; Université Paris-Sud, 91405 Orsay, France. Electronic address:

Chimeric transcription factors are a hallmark of human leukemia, but the molecular mechanisms by which they block differentiation and promote aberrant self-renewal remain unclear. Here, we demonstrate that the ETO2-GLIS2 fusion oncoprotein, which is found in aggressive acute megakaryoblastic leukemia, confers megakaryocytic identity via the GLIS2 moiety while both ETO2 and GLIS2 domains are required to drive increased self-renewal properties. ETO2-GLIS2 directly binds DNA to control transcription of associated genes by upregulation of expression and interaction with the ETS-related ERG protein at enhancer elements. Read More

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GATA factor mutations in hematologic disease.

Blood 2017 04 8;129(15):2103-2110. Epub 2017 Feb 8.

Department of Pathology, University of Washington School of Medicine, Seattle, WA.

GATA family proteins play essential roles in development of many cell types, including hematopoietic, cardiac, and endodermal lineages. The first three factors, GATAs 1, 2, and 3, are essential for normal hematopoiesis, and their mutations are responsible for a variety of blood disorders. Acquired and inherited mutations contribute to Diamond-Blackfan anemia, acute megakaryoblastic leukemia, transient myeloproliferative disorder, and a group of related congenital dyserythropoietic anemias with thrombocytopenia. Read More

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Sometimes it is better to wait: First Italian case of a newborn with transient abnormal myelopoiesis and a favorable prognosis.

Oncol Lett 2017 Jan 21;13(1):191-195. Epub 2016 Nov 21.

Department of Hematology, Bambino Gesù Children's Hospital, I-00165 Rome, Italy.

Congenital leukemia is rare disease with an incidence of one to five cases per million births. Transient abnormal myelopoiesis (TAM), also called transient myeloproliferative disorder, is a pre-leukemia disorder that may occur in Down syndrome (DS) or non-DS infants. TAM may enter spontaneous remission; however, continual monitoring is required, as this disorder has been observed to develop into acute megakaryoblastic leukemia in 16-30% of cases. Read More

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January 2017

Prognostic impact of specific molecular profiles in pediatric acute megakaryoblastic leukemia in non-Down syndrome.

Genes Chromosomes Cancer 2017 05 14;56(5):394-404. Epub 2017 Feb 14.

Department of Hematology and Oncology, Gunma Children's Medical Center, Shibukawa, Japan.

Pediatric acute megakaryoblastic leukemia in non-Down syndrome (AMKL) is a unique subtype of acute myeloid leukemia (AML). Novel CBFA2T3-GLIS2 and NUP98-KDM5A fusions recurrently found in AMKL were recently reported as poor prognostic factors. However, their detailed clinical and molecular characteristics in patients treated with recent improved therapies remain uncertain. Read More

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Distinct GATA1 Point Mutations in Monozygotic Twins With Down Syndrome and Transient Abnormal Myelopoiesis From a Triplet Pregnancy: A Case Report and Review of Literature.

Am J Clin Pathol 2016 Dec 27;146(6):753-759. Epub 2016 Dec 27.

From the Department of Pathology, University of Colorado, Anschutz Medical Campus, Aurora

Objectives: Down syndrome (DS)-associated transient abnormal myelopoiesis (TAM) or acute megakaryoblastic leukemia (AMKL) in monozygotic twins is exceedingly rare and has not been well characterized.

Methods: We describe a unique case of monozygotic twins with simultaneous TAM from a triplet pregnancy at 34 weeks' gestation. Previously reported cases of TAM and DS-AMKL in monozygotic twins have been reviewed to compare with our cases. Read More

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December 2016

A neonate with a unique non-Down syndrome transient proliferative megakaryoblastic disease.

Pediatr Blood Cancer 2017 03 26;64(3). Epub 2016 Sep 26.

Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands.

Transient myeloproliferative disorder (TMD) is a leukemia type that occurs typically in newborns. In Down syndrome, TMD is referred to as transient abnormal myelopoiesis (TAM). Recently, transientness has also been reported in acute myeloid leukemia patients with germline trisomy 21 mosaicism, and even in cases with somatic trisomy 21, with or without GATA1 mutations. Read More

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Evolution of myeloid leukemia in children with Down syndrome.

Satoshi Saida

Int J Hematol 2016 Apr 24;103(4):365-72. Epub 2016 Feb 24.

Department of Pediatrics, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, 606-8507, Japan.

Children with Down syndrome (DS) have a markedly increased risk of leukemia. They are at particular risk of acute megakaryoblastic leukemia, known as myeloid leukemia associated with DS (ML-DS), the development of which is closely linked to a preceding temporary form of neonatal leukemia called transient abnormal myelopoiesis (TAM). Findings from recent clinical and laboratory studies suggest that constitutional trisomy 21 and GATA1 mutation(s) cause TAM, and that additional genetic alteration(s) including those in epigenetic regulators and signaling molecules are involved in the progression from TAM to ML-DS. Read More

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Down syndrome and leukemia: insights into leukemogenesis and translational targets.

Transl Pediatr 2015 Apr;4(2):76-92

1 Kids Cancer Centre, Sydney Children's Hospital, Randwick, Australia ; 2 School of Women's and Children's Health, University of New South Wales, Kensington, Australia ; 3 Children's Cancer Institute Australia, University of New South Wales, Lowy Cancer Centre, Randwick, Australia.

Children with Down syndrome (DS) have a significantly increased risk of childhood leukemia, in particular acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic leukemia (DS-ALL). A pre-leukemia, called transient myeloproliferative disorder (TMD), characterised by a GATA binding protein 1 (GATA1) mutation, affects up to 30% of newborns with DS. In most cases, the pre-leukemia regresses spontaneously, however one-quarter of these children will go on to develop AMKL or myelodysplastic syndrome (MDS) . Read More

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Long-term outcome for Down syndrome patients with hematopoietic disorders.

J Formos Med Assoc 2016 Feb 30;115(2):94-9. Epub 2015 Jul 30.

Department of Pediatrics, National Taiwan University Hospital and College of Medicine, National Taiwan University, Taipei, Taiwan. Electronic address:

Background/purpose: Although Down syndrome (DS) patients have a higher risk of developing transient myeloproliferative disorder (TMD) and acute leukemia, very little data is available on long-term outcome in Taiwanese patients. The current study was designed to determine the clinical characteristics and treatment outcome of DS patients with TMD or acute leukemia (AL).

Methods: In 25 consecutive DS patients with TMD or AL enrolled from 1990 to 2012, clinical manifestations and treatment protocols were investigated and GATA1 (GATA binding protein 1) mutations were identified. Read More

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February 2016

Acute megakaryocytic leukemia: What have we learned.

Blood Rev 2016 Jan 18;30(1):49-53. Epub 2015 Jul 18.

Department of Hematology/Oncology, The West Cancer Center, USA.

Acute megakaryocytic leukemia (AMegL) is a biologically heterogenous subtype of acute myeloid leukemia (AML) that arises from megakaryocytes. Improvements in the accuracy of diagnosing AMegL as well as interest in the molecular analysis of leukemias have led to an increased amount of data available on this rare AML subtype. In this review, we will analyze the diverse molecular features unique to AMegL and how they have influenced the development of novel treatment strategies, including polyploidization. Read More

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January 2016

Presentation of Acute Megakaryoblastic Leukemia Associated with a GATA-1 Mutation Mimicking the Eruption of Transient Myeloproliferative Disorder.

Pediatr Dermatol 2015 Sep-Oct;32(5):e204-7. Epub 2015 Jul 23.

Section of Dermatology, Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.

Children with trisomy 21 are prone to developing hematologic disorders, including transient myeloproliferative disorder (TMD) and acute megakaryoblastic leukemia (AMKL). The papulovesicular eruption of TMD provides an important clue to the diagnosis. In contrast, AMKL rarely has associated cutaneous findings. Read More

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The biology of pediatric acute megakaryoblastic leukemia.

Blood 2015 Aug 17;126(8):943-9. Epub 2015 Jul 17.

Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN.

Acute megakaryoblastic leukemia (AMKL) comprises between 4% and 15% of newly diagnosed pediatric acute myeloid leukemia patients. AMKL in children with Down syndrome (DS) is characterized by a founding GATA1 mutation that cooperates with trisomy 21, followed by the acquisition of additional somatic mutations. In contrast, non-DS-AMKL is characterized by chimeric oncogenes consisting of genes known to play a role in normal hematopoiesis. Read More

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