• KOL
    • Sideroblastic Anemia
    • Mark D Fleming
    • Mark D Fleming: Influence Statistics

      Mark D Fleming

      Mark D Fleming

      Department of Pathology, Boston Children’s Hospital, Harvard Medical School, Boston, United States of America | Department of Pathology, Boston Children’s Hospital, Harvard ...

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      Mark D Fleming:Expert Impact

      Concepts for whichMark D Fleminghas direct influence:Sideroblastic anemia,Iron deficiency,Iron overload,Myelodysplastic syndrome,Iron transport,Hepcidin expression,Acute myeloid leukaemia,Bone marrow.

      Mark D Fleming:KOL impact

      Concepts related to the work of other authors for whichfor which Mark D Fleming has influence:Cancer cells,Iron metabolism,Gene expression,Pyruvate kinase,Oxidative stress,Ewing sarcoma,Langerhans cell histiocytosis.

      KOL Resume for Mark D Fleming

      Year
      2022

      Department of Pathology, Boston Children’s Hospital, Harvard Medical School, Boston, United States of America

      2021

      Boston Children’s Hospital, Boston, MA, USA

      2020

      Harvard Medical School, Boston, MA, USA

      Department of Pathology, Boston Children's Hospital, Boston, MA.

      2019

      Department of Pathology, Boston Children's Hospital, Boston, Massachusetts

      Harvard Medical School, Boston, MA

      2018

      Department of Pathology, Boston Children's Hospital, Boston, MA

      Boston Children Hospital;

      2017

      Department of Pathology, Boston Children’s Hospital, and

      Boston Children’s Hospital, Boston, MA

      2016

      Department of Pathology, Boston Children's Hospital, Boston, MA 02115, USA

      2015

      Department of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, MA.

      Mayo Clinic, Rochester, Minnesota.

      2014

      Department of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.

      Boston Children's Hospital, Boston, MA

      2013

      Department of Pathology, Children’s Hospital Boston, Harvard Medical School, Boston, MA 02115, USA

      2012

      Department of Pathology, Children's Hospital Boston, MA, USA

      2011

      Pediatrics, and

      Departments of Pathology,

      Children's Hospital Boston, Boston, MA

      2010

      Department of Pathology, Children's Hospital, Boston, Massachusetts

      Pathology, Children's Hospital Boston, Harvard Medical School, Boston, MA, USA,

      Enders 1116.1, Children's Hospital, 300 Longwood Ave, Boston, MA 02115

      2009

      Pathology, Children's Hospital Boston, Harvard Medical School, Boston, MA, USA

      James V. Neel Distinguished University Professor, Departments of Internal Medicine, Pediatrics and Communicable Diseases, and Human Genetics, Investigator, Howard Hughes Medical Institute, University of Michigan Medical School, Ann Arbor, Michigan

      Professor of Pediatrics, Edward Wigglesworth Professor of Dermatology, Harvard Medical School, Chief, Department of Dermatology, Massachusetts General Hospital, Boston, Massachusetts

      2008

      Department of Pathology, Children’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA

      Mark Fleming, Associate Professor of Pathology, Children’s Hospital, Harvard Medical School, Enders 1116.1, 300 Longwood Ave, Boston, MA 02115; e-mail: mark.fleming{at}childrens.harvard.edu ; Mark Fleming, Associate Professor of Pathology, Children’s Hospital, Harvard Medical School, Enders 1116.1, 300 Longwood Ave, Boston, MA 02115; e-mail: mark.fleming{at}childrens.harvard.edu

      2007

      Department of Pathology, Children's Hospital and Harvard Medical School, Boston, MA;

      Children’s Hospital Boston, Harvard Medical School, Boston, MA, USA

      Sample of concepts for which Mark D Fleming is among the top experts in the world.
      Concept World rank
      eif6 mutations #1
      chain anemia #1
      clinical surveillance shwachman #1
      repressing iron #1
      mlasa2 yars2 #1
      iron overload tfhpx #1
      16 myelodysplasia #1
      subacute gastrointestinal hemorrhage #1
      erythroblast mitochondria pathogenesis #1
      quantification hepcidin #1
      abcb7 slc19a2 #1
      porphyrin insufficiency #1
      linked hematopoiesis #1
      basal bmp alk2 #1
      ferrireductases vivo #1
      cd19⁺ range #1
      trflike protein #1
      2 alas2 families #1
      trnt1 homolog #1
      epp hri #1
      tmprss6 mutation status #1
      hri deficiency epp #1
      hrg1 haem #1
      recurrent febrile illness #1
      review hepcidin regulation #1
      slc25a38 abcb7 #1
      mouse strain generations #1
      deficient hjv #1
      protein belgrade rat #1
      researchers heme transporters #1
      arg216gln mutation #1
      mark samuels colleagues #1
      pus1 abcb7 #1
      gata1 gps #1
      abcb7 essential #1
      mutations irida #1
      abcb7 xlsa #1
      lnptmprss6 sirna treatment #1
      proteins sod2deficient cells #1
      chromosome 5 males #1
      transferrin iron syncytiotrophoblast #1
      compensatory clonal #1
      sirt3 transferrin sirtuin #1
      transferrin hepcidin mimetics #1
      mutations mark samuels #1
      oncogenic nras allele #1
      hemoproteins iron recycling #1
      heme biosynthesis pathways #1
      yars2 variant #1

      Prominent publications by Mark D Fleming

      KOL-Index: 13922

      Bone morphogenetic protein (BMP) signaling induces hepatic expression of the peptide hormone hepcidin. Hepcidin reduces serum iron levels by promoting degradation of the iron exporter ferroportin. A relative deficiency of hepcidin underlies the pathophysiology of many of the genetically distinct iron overload disorders, collectively termed hereditary hemochromatosis. Conversely, chronic inflammatory conditions and neoplastic diseases can induce high hepcidin levels, leading to impaired ...

      Known for Bmp Type | Iron Overload | Hepcidin Expression | Alk2 Alk3 | Mice Mice
      KOL-Index: 13796

      Iron-refractory, iron-deficiency anemia (IRIDA) is a familial disorder characterized by iron deficiency anemia unresponsive to oral iron treatment but partially responsive to intravenous iron therapy. Previously, we showed that IRIDA patients harbor loss-of-function mutations in TMPRSS6, a type II transmembrane serine protease primarily expressed by the liver. Both humans and mice with TMPRSS6 mutations show inappropriately elevated levels of the iron-regulatory hormone hepcidin, ...

      Known for Systemic Iron Homeostasis | Bmp Smad | Mice Tmprss6 | Hepcidin Expression | Knockout Rna
      KOL-Index: 12673

      The Belgrade (b) rat has an autosomal recessively inherited, microcytic, hypochromic anemia associated with abnormal reticulocyte iron uptake and gastrointestinal iron absorption. The b reticulocyte defect appears to be failure of iron transport out of endosomes within the transferrin cycle. Aspects of this phenotype are similar to those reported for the microcytic anemia (mk) mutation in the mouse. Recently, mk has been attributed to a missense mutation in the gene encoding the putative ...

      Known for Iron Transport | Nramp2 Protein | Mk Mouse | Microcytic Anemia | Transferrin Cycle
      KOL-Index: 12387

      It has been suggested that a switch in chemokine receptor expression underlies Langerhans cell migration from skin to lymphoid tissue. Activated cells are thought to down-regulate CCR6, whose ligand macrophage inflammatory protein-3 alpha (MIP-3 alpha)/CCL20 is expressed in skin, and up-regulate CCR7, whose ligands are in lymphoid tissues. In Langerhans cell histiocytosis (LCH), pathologic Langerhans cells (LCs) accumulate in several tissues, including skin, bone, and lymphoid organs. We ...

      Known for Langerhans Cell Histiocytosis | Chemokine Receptors | Ccr6 Ccr7 | Skin Bone | Lymphoid Tissues
      KOL-Index: 12297

      Patients with hematologic malignancies undergoing allogeneic stem cell transplantation (HSCT) commonly have an elevated serum ferritin prior to HSCT, which has been associated with increased mortality after transplantation. This has led to the suggestion that iron overload is common and deleterious in this patient population. However, the relationship between serum ferritin and parenchymal iron overload in such patients is unknown. We report a prospective study of 48 patients with acute ...

      Known for Acute Leukemia | Iron Overload | Cell Transplantation | Serum Ferritin | Myelodysplastic Syndromes
      KOL-Index: 12173

      BACKGROUND: Sideroblastic anemias are heterogeneous congenital and acquired bone marrow disorders characterized by pathologic iron deposits in mitochondria of erythroid precursors. Among the congenital sideroblastic anemias (CSAs), the most common form is X-linked sideroblastic anemia, due to mutations in 5-aminolevulinate synthase (ALAS2). A novel autosomal recessive CSA, caused by mutations in the erythroid specific mitochondrial transporter SLC25A38, was recently defined. Other known ...

      Known for Congenital Sideroblastic Anemia | Sideroblastic Child Child | Alas2 Slc25a38 | Mitochondrial Membrane | Common Form
      KOL-Index: 11723

      KRAS is often mutated in human hematopoietic malignancies, including juvenile myelomonocytic leukemia (JMML) and T-cell lymphoblastic leukemia/lymphoma (TLL/L). However, the exact role and function of oncogenic KRAS mutations in the initiation and progression of JMML and TLL/L remain elusive. Here, we report the use of a mouse bone marrow transplantation model to study oncogenic Kras-induced leukemogenesis. We show that as the first genetic hit, oncogenic Kras mutations initiate both ...

      Known for Oncogenic Kras | Stem Cell | Myeloid Progenitors | Solid Tumors | Transformation Neoplastic
      KOL-Index: 11251

      We describe the cloning of p63, a gene at chromosome 3q27-29 that bears strong homology to the tumor suppressor p53 and to the related gene, p73. p63 was detected in a variety of human and mouse tissues, including proliferating basal cells of epithelial layers in the epidermis, cervix, urothelium, and prostate. Unlike p53, the p63 gene encodes multiple isotypes with remarkably divergent abilities to transactivate p53 reporter genes and induce apoptosis. Importantly, the predominant p63 ...

      Known for P53 Homolog | Tumor Suppressor Genes | Situ Hybridization | Encodes Multiple | Proteins Mice
      KOL-Index: 11201

      Hereditary hemochromatosis, which is characterized by inappropriately low levels of hepcidin, increased dietary iron uptake, and systemic iron accumulation, has been associated with mutations in the HFE, transferrin receptor-2 (TfR2), and hemojuvelin (HJV) genes. However, it is still not clear whether these molecules intersect in vivo with bone morphogenetic protein 6 (BMP6)/mothers against decapentaplegic (SMAD) homolog signaling, the main pathway up-regulating hepcidin expression in ...

      Known for Iron Phenotype | Morphogenetic Protein | Bmp6 Hjv | Hepcidin Expression Response | Deficient Mice
      KOL-Index: 11083

      Proteins with iron-sulfur (Fe-S) clusters participate in multiple metabolic pathways throughout the cell. The mitochondrial ABC half-transporter Abcb7, which is mutated in X-linked sideroblastic anemia with ataxia in humans, is a functional ortholog of yeast Atm1p and is predicted to export a mitochondrially derived metabolite required for cytosolic Fe-S cluster assembly. Using an inducible Cre/loxP system to delete exons 9 and 10 of the Abcb7 gene, we examined the phenotype of mice ...

      Known for Cytosolic Iron | Sulfur Cluster | Binding Cassette | Mitochondrial Atp | Transporter Abcb7
      KOL-Index: 11033

      A number of genetic mutations have been identified in human breast cancers, yet the specific combinations of mutations required in concert to form breast carcinoma cells remain unknown. One approach to identifying the genetic and biochemical alterations required for this process involves the transformation of primary human mammary epithelial cells (HMECs) to carcinoma cells through the introduction of specific genes. Here we show that introduction of three genes encoding the SV40 large-T ...

      Known for Human Breast | Mammary Epithelial | Oncogenic Transformation | Cells Tumors | Tumor Formation
      KOL-Index: 10744

      Although the physiological role of tissue-specific translational control of gene expression in mammals has long been suspected on the basis of biochemical studies, direct evidence has been lacking. Here, we report on the targeted disruption of the gene encoding the heme-regulated eIF2alpha kinase (HRI) in mice. We establish that HRI, which is expressed predominantly in erythroid cells, regulates the synthesis of both alpha- and beta-globins in red blood cell (RBC) precursors by ...

      Known for Erythroid Precursors | Translational Regulation | Iron Deficiency | Eif2α Kinase | Cell Survival
      KOL-Index: 10743

      Microcytic anemia (mk) mice and Belgrade (b) rats have severe iron deficiency anemia due to defects in intestinal iron transport and erythroid iron utilization. Both animal mutants carry the same missense mutation in Nramp2, the first mammalian iron transporter to be identified. This mutation, in which glycine 185 is changed to arginine (G185R), occurs within predicted transmembrane domain 4 of the protein. We have performed site-directed mutagenesis of murine Nramp2, focusing on amino ...

      Known for Iron Transport | G185r Mutation | Cultured Cloning | Transmembrane Domain | Nramp2 Function
      KOL-Index: 10620

      Oncogenic NRAS mutations are frequently identified in myeloid diseases involving monocyte lineage. However, its role in the genesis of these diseases remains elusive. We report a mouse bone marrow transplantation model harboring an oncogenic G12D mutation in the Nras locus. Approximately 95% of recipient mice develop a myeloproliferative disease resembling the myeloproliferative variant of chronic myelomonocytic leukemia (CMML), with a prolonged latency and acquisition of multiple ...

      Known for Oncogenic Nras | Chronic Myelomonocytic | Csf Signaling | Murine Model | Cmml Cells

      Key People For Sideroblastic Anemia

      Top KOLs in the world
      #1
      Sylvia S Bottomley
      sideroblastic anemia iron overload heme biosynthesis
      #2
      David F Bishop
      fabry disease uroporphyrinogen iii synthase acute intermittent porphyria
      #3
      Alison May
      sideroblastic anaemia prenatal diagnosis iron overload
      #4
      Mark D Fleming
      sideroblastic anemia iron deficiency myelodysplastic syndrome
      #5
      Philip D Cotter
      situ hybridization prenatal diagnosis human pair
      #6
      Dean R Campagna
      sideroblastic anemia gata2 mutations iron deficiency

      Department of Pathology, Boston Children’s Hospital, Harvard Medical School, Boston, United States of America | Department of Pathology, Boston Children’s Hospital, Harvard Medical School, Boston, MA; | Department of Pathology, Boston Children's Hosp

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