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    • Bone Marrow
    • Colin A Sieff
    • Colin A Sieff: Influence Statistics

      Colin A Sieff

      Colin A Sieff

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      Cancer and Blood Disorders Center, Dana-Farber Cancer Center and Boston Children's Hospital, and Department of Pediatrics, Harvard Medical School, Boston, MA 02115. | Harvard ...

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      Colin A Sieff:Expert Impact

      Concepts for whichColin A Sieffhas direct influence:Bone marrow,Blackfan anemia,Stimulating factor,Mesenchymal cells,Dba patients,Ribosomal protein,Macrophage colony,Rp genes.

      Colin A Sieff:KOL impact

      Concepts related to the work of other authors for whichfor which Colin A Sieff has influence:Stem cells,Bone marrow,Stimulating factor,Blackfan anemia,Ribosomal protein,Macrophage colony,Host disease.

      KOL Resume for Colin A Sieff

      Year
      2021

      Cancer and Blood Disorders Center, Dana-Farber Cancer Center and Boston Children's Hospital, and Department of Pediatrics, Harvard Medical School, Boston, MA 02115.

      2020

      Harvard Medical School, Dana‐Farber and Boston Children's, Cancer and Blood Disorders Center, Boston, Massachusetts

      2019

      Harvard Medical School, Dana-Farber and Boston Children's, Cancer and Blood Disorders Center, Boston, Massachusetts, USA.

      2018

      Division of Hematology/Oncology, Dana-Farber and Boston Children’s Cancer and Blood Disorders Center, Dana 3104, 450 Brookline Avenue, Boston, MA 02215, USA

      Dana-Farber Cancer Institute, Boston Children's Cancer and Blood Disorders Center, Boston, MA

      2017

      Harvard Medical School, Boston, MA 02115, USA.

      2016

      Boston Children's Hospital, Boston, USA

      2015

      Division of Hematology, Boston Children's Hospital, Boston, Massachusetts, USA.

      2014

      Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115, USA

      2013

      Division of Pediatric Hematology, Boston Children’s Hospital, Boston, MA, USA

      2012

      Division of Pediatric Hematology, Children's Hospital Boston, Boston, Massachusetts

      2010

      Harvard Medical School, Boston, MA 02115, USA

      2009

      Division of Pediatric Hematology, Children's Hospital Boston, Harvard Medical School, Boston, MA, USA,

      Department of Hematology/Oncology, Childrens Hospital Boston, Boston, MA, USA

      Whitehead Institute for Biomedical Research, Cambridge

      2008

      Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA;

      2007

      Division of Pediatric Hematology, Children’s Hospital Boston, Boston, MA, USA

      2006

      Division of Pediatric Hematology, Harvard Medical School, Boston

      2005

      Division of Pediatric Hematology and Oncology, Dana-Farber Cancer Institute and Children's Hospital, Boston, MA 02115, USA

      From the Departments of Medical Oncology and Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA; and the Broad Institute of Harvard and Massachusetts Institute of Technology (MIT), Cambridge, MA

      Department of Pediatric Oncology and Hematology, Dana‐Farber Cancer Institute, Boston, Massachusetts

      2004

      Department of Pediatric Oncology, Dana Farber Cancer Institute, Boston

      2000

      Departments of Pediatric Oncology, Harvard Medical School, Boston, Massachusetts, USA

      Division of Paediatric 
Hematology and Oncology,

      1999

      Department of Hematology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115

      1998

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

      1997

      Colin Sieff, MB, ChB, Associate Professor of Pediatrics, Department of Pediatric Oncology, Dana Farber Cancer Institute

      1996

      Division of Pediatric Hematology, Harvard Medical School, Boston, MA, USA.

      the Joslin Diabetes Center and Harvard Medical School, Boston, Massachusetts 02115

      Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA

      1995

      Colin A. Sieff, MB, BCh, Associate Professor, Pediatric Oncology, Department of Pediatrics, Dana-Farber Cancer Institute

      Division of Hematology-Oncology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.

      1994

      Division of Hematology and Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.

      1993

      Dana‐Farber Cancer Institute, 44 Binney Street, Room Dana 1630B, Boston, MA 02115, USA

      Division of Pediatric Hematology and Oncology, Dana-Farber Cancer Institute, Boston, MA 02115.

      1992

      Division of Pediatric Hematology and Oncology and Howard Hughes Medical Institute, Department of Medicine and Division of Biostatistics, Children's Hospital and Dana‐Farber Cancer Institute, Boston, Mass.: Department of Pediatrics. Harvard Medical School, Boston. Mass.: Amgen Inc., Thousand Oaks, Calif.; and the Herman B Wells Center for Pediatric Research and Howard Hughes Medical Institute, Indiana University School of Medicine. Indianapolis. Ind

      1991

      Division of Hematology, Brigham and Women's Hospital, Boston, MA.

      Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.

      1990

      Division of Hematology and Oncology, Dana Farber Cancer Institute, Boston, Massachusetts.

      1989

      Department of Medicine, Dana-Farber Cancer Institute, Boston, MA 02115.

      Division of Pediatric Oncology and Hematology, Dana-Farber Cancer Institute, Boston.

      1988

      Division of Hematology and Pediatric Oncology, Children's Hospital, Boston, MA 02115.

      Children's Hospital, Dana-Farber Cancer Institute, Harvard University, Boston, Massachusetts, USA.

      1987

      Division of Pediatric Oncology, Children's Hospital, Boston, MA.

      1986

      The Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 02115

      Department of Pediatric Oncology Dana-Farber Cancer Institute Boston, Massachusetts, USA

      1985

      Division of Hematology and Oncology, Children's Hospital, and Dana-Farber Cancer Institute; Division of Hematology, Brigham and Women's Hospital; and Departments of Pediatrics and Medicine, Harvard Medical School, Boston, Massachusetts 02115

      Sign-in to see all concepts, it's free!
      Sample of concepts for which Colin A Sieff is among the top experts in the world.
      Concept World rank
      specific hgfs #1
      cats dba #1
      steroid treatment nonresponders #1
      rps19 transcript #1
      ribosomal protein 25 #1
      blackfan anemia dba #1
      new 84aminoacid sequence #1
      older p55 mice #1
      messenger receptors mds #1
      nonresponders transfusion #1
      hypoplasia fanconi anemia #1
      diamondblackfan chromosomes #1
      dba early infancy #1
      animal erythropoiesis humans #1
      27kd isoform #1
      79base intron insertion #1
      decreased rps19 #1
      head upper limbs #1
      reported patients disease #1
      impaired beta expression #1
      cytoplasmic truncation mutants #1
      drug remissions #1
      nonadherent cell production #1
      vivo p55 subunit #1
      erythropoiesis low doses #1
      diamondblackfan chromosomes human #1
      p55 marrow #1
      beta mds #1
      intron‐retained mrna #1
      abnormal beta transcripts #1
      chain neutrophils #1
      age matched p75 #1
      broad developmental disease #1
      beta c79 #1
      quarter reported patients #1
      prednisone erythropoiesis #1
      rps19 dba #1
      Sign-in to see all concepts, it's free!

      Prominent publications by Colin A Sieff

      KOL-Index: 13017

      Diamond-Blackfan anemia (DBA), a congenital erythroblastopenia, is a model disease for the study of erythroid differentiation but is poorly understood. RPS19 is the only gene yet to have been associated with DBA, but its relevance to erythroid differentiation is unclear. The molecular basis for the stimulation of erythropoiesis by glucocorticoids in patients with DBA has not been identified. We demonstrate that targeted degradation of the RPS19 transcript, through retroviral expression ...

      Known for Blackfan Anemia | Rps19 Deficiency | Rna Interference | Erythroid Differentiation | Molecular Basis
      KOL-Index: 12323

      Granulocyte-macrophage colony-stimulating factor (GM-CSF) regulates the growth and function of several myeloid cell types at different stages of maturation. The effects of GM-CSF are mediated through a high affinity receptor that is composed of two chains: a unique, ligand-specific alpha chain and a beta common chain (beta c) that is also a component of the receptors for interleukin 3 (IL-3) and IL-5. Beta c plays an essential role in the transduction of extra cellular signals to the ...

      Known for Stimulating Factor | Macrophage Colony | Ptb Domain | Tyrosine Phosphorylation | Gm Csf
      KOL-Index: 12063

      Diamond-Blackfan anemia (DBA), an inherited bone marrow failure syndrome characterized by anemia that usually presents before the first birthday or in early childhood, is associated with birth defects and an increased risk of cancer. Although anemia is the most prominent feature of DBA, the disease is also characterized by growth retardation and congenital malformations, in particular craniofacial, upper limb, heart, and urinary system defects that are present in approximately 30%-50% of ...

      Known for Ribosomal Protein | Blackfan Anemia | Rps10 Rps26 | Dba Mutations | Rp Genes
      KOL-Index: 11786

      Diamond-Blackfan anemia (DBA), a congenital bone-marrow-failure syndrome, is characterized by red blood cell aplasia, macrocytic anemia, clinical heterogeneity, and increased risk of malignancy. Although anemia is the most prominent feature of DBA, the disease is also characterized by growth retardation and congenital anomalies that are present in approximately 30%-50% of patients. The disease has been associated with mutations in four ribosomal protein (RP) genes, RPS19, RPS24, RPS17, ...

      Known for Cleft Palate | Anemia Patients | Rpl5 Rpl11 | Ribosomal Protein L5 | Rp Genes
      KOL-Index: 11642

      Human granulocyte-macrophage colony-stimulating factor (GM-CSF) has been shown to inhibit migration of mature granulocytes and to enhance their antibody-dependent cellular cytotoxicity. We found that human recombinant GM-CSF also enhanced granulocyte-granulocyte adhesion and increased by two- to threefold the surface expression of Mo1 and LeuM5 (P150, 95), two members of a family of leukocyte adhesion molecules (Leu-CAM). Increased Mo1 surface expression occurred within 15 min at 37 ...

      Known for Cell Adhesion | Surface Expression | Recombinant Granulocyte | Gm Csf | Macrophage Colony
      KOL-Index: 11493

      We previously described a method for isolating murine hematopoietic stem cells capable of reconstituting lethally irradiated recipients, which depends solely on dual-wavelength flow cytometric analysis of murine bone marrow cells stained with the fluorescent DNA-binding dye Hoechst 33342. This method, which appears to rely on the differential ability of stem cells to efflux the Hoechst dye, defines an extremely small and homogeneous population of cells (termed SP cells). We show here ...

      Known for Stem Cells | Cd34 Antigen | Dye Efflux | Multiple Species | Murine Hematopoietic
      KOL-Index: 10742

      Diamond-Blackfan anemia (DBA) is an inherited bone marrow failure syndrome characterized by anemia, congenital abnormalities, and cancer predisposition. Small ribosomal subunit genes RPS19, RPS24, and RPS17 are mutated in approximately one-third of patients. We used a candidate gene strategy combining high-resolution genomic mapping and gene expression microarray in the analysis of 2 DBA patients with chromosome 3q deletions to identify RPL35A as a potential DBA gene. Sequence analysis ...

      Known for Ribosomal Subunit | Blackfan Anemia | Posttranscriptional Rna | Sequence Analysis | Cancer Predisposition
      KOL-Index: 10651

      Adenovirus vectors have been used to transfer genes into both hematopoietic progenitor cells and tumor cells, including carcinoma cells that have metastasized to bone marrow (BM). However, the relative susceptibility of different subsets of hematopoietic cells is unknown. In permissive cells adenoviral-mediated gene transfer is mediated by the coxsackievirus and adenovirus receptor (CAR) protein and alpha(v) integrins expressed on the cell surface of the target cells. This prompted us to ...

      Known for Hematopoietic Cells | Car Expression | Gene Transfer | Cell Surface | Adenovirus Receptor
      KOL-Index: 10444

      Diamond-Blackfan anemia (DBA) is a broad developmental disease characterized by anemia, bone marrow (BM) erythroblastopenia, and an increased incidence of malignancy. Mutations in ribosomal protein gene S19 (RPS19) are found in approximately 25% of DBA patients; however, the role of RPS19 in the pathogenesis of DBA remains unknown. Using global gene expression analysis, we compared highly purified multipotential, erythroid, and myeloid BM progenitors from RPS19 mutated and control ...

      Known for Ribosomal Protein | Blackfan Anemia | Gene Expression | Rps19 Mutations | Erythroid Cells
      KOL-Index: 10363

      BACKGROUND: Peripheral blood progenitor cells, harvested by apheresis after mobilization, provide rapid hematologic recovery after high-dose chemotherapy. However, because harvesting these cells is expensive and time-consuming, there has been much interest in optimizing collection protocols. An investigation was made to determine whether, in this clinical setting, peripheral blood progenitor cell yields may be predicted from preapheresis progenitor cell counts, allowing the length of ...

      Known for Cell Counts | Blood Cd34 | Preapheresis Peripheral | Hematopoietic Stem | Stimulating Factor
      KOL-Index: 10253

      Hematopoietic stem cell (HSC) self-renewal is a complicated process, and its regulatory mechanisms are poorly understood. Previous studies have identified tumor necrosis factor (TNF)-alpha as a pleiotropic cytokine, which, among other actions, prevents various hematopoietic progenitor cells from proliferating and differentiating in vitro. However, its role in regulating long-term repopulating HSCs in vivo has not been investigated. In this study, mice deficient for the p55 or the p75 ...

      Known for Tumor Necrosis Factor | Stem Cell | Knockout Receptors | C57bl Mice | Tnf Receptor

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      Cancer and Blood Disorders Center, Dana-Farber Cancer Center and Boston Children's Hospital, and Department of Pediatrics, Harvard Medical School, Boston, MA 02115. | Harvard Medical School, Dana‐Farber and Boston Children's, Cancer and Blood Disorde

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