The Experts below are selected from a list of 63 Experts worldwide ranked by ideXlab platform

Paul A. Ney - One of the best experts on this subject based on the ideXlab platform.

  • HEMATOPOIESIS Role of erythropoietin receptor signaling in Friend virus–induced Erythroblastosis and polycythemia
    2016
    Co-Authors: Ji Zhang, Melanie R. Loyd, Rachel L. Schweers, Derek A. Persons, Jerold E. Rehg, Constance T. Noguchi, James N. Ihle, Mindy S. R, Paul A. Ney
    Abstract:

    Friend virus is an acutely oncogenic retro-virus that causes Erythroblastosis and polycythemia in mice. Previous studies suggested that the Friend virus oncopro-tein, gp55, constitutively activates the erythropoietin receptor (EPOR), causing uncontrolled erythroid proliferation. Those studies showed that gp55 confers growth factor independence on an inter-leukin-3 (IL-3)–dependent cell line (Ba/F3) when the EPOR is coexpressed. Subse-quently, we showed that a truncated form of the stem-cell kinase receptor (sf-STK) is required for susceptibility to Friend disease. Given the requirement for sf-STK, we sought to establish the in vivo signifi-cance of gp55-mediated activation of the EPOR. We found that the cytoplasmic tyrosine residues of the EPOR, and signal transducer and activator of transcrip-tion-5 (STAT5), which acts through these sites, are not required for Friend virus– induced Erythroblastosis. The EPOR itself was required for the development of eryth-roblastosis but not for gp55-mediated ery-throid proliferation. Interestingly, the mu-rine EPOR, which is required for gp55-mediated Ba/F3-cell proliferation, was dispensable for Erythroblastosis in vivo. Finally, gp55-mediated activation of the EPOR and STAT5 are required for Friend virus–induced polycythemia. These results suggest that Friend virus activates both sf-STK and the EPOR to cause deregulated erythroid proliferation and differentiation

  • Role of erythropoietin receptor signaling in Friend virus-induced Erythroblastosis and polycythemia
    Blood, 2005
    Co-Authors: Ji Zhang, Mindy S. Randall, Melanie R. Loyd, Rachel L. Schweers, Derek A. Persons, Jerold E. Rehg, Constance T. Noguchi, James N. Ihle, Paul A. Ney
    Abstract:

    Friend virus is an acutely oncogenic retrovirus that causes Erythroblastosis and polycythemia in mice. Previous studies suggested that the Friend virus oncoprotein, gp55, constitutively activates the erythropoietin receptor (EPOR), causing uncontrolled erythroid proliferation. Those studies showed that gp55 confers growth factor independence on an interleukin-3 (IL-3)-dependent cell line (Ba/F3) when the EPOR is coexpressed. Subsequently, we showed that a truncated form of the stem-cell kinase receptor (sf-STK) is required for susceptibility to Friend disease. Given the requirement for sf-STK, we sought to establish the in vivo significance of gp55-mediated activation of the EPOR. We found that the cytoplasmic tyrosine residues of the EPOR, and signal transducer and activator of transcription-5 (STAT5), which acts through these sites, are not required for Friend virus-induced Erythroblastosis. The EPOR itself was required for the development of Erythroblastosis but not for gp55-mediated erythroid proliferation. Interestingly, the murine EPOR, which is required for gp55-mediated Ba/F3-cell proliferation, was dispensable for Erythroblastosis in vivo. Finally, gp55-mediated activation of the EPOR and STAT5 are required for Friend virus-induced polycythemia. These results suggest that Friend virus activates both sf-STK and the EPOR to cause deregulated erythroid proliferation and differentiation.

Joseph Lau - One of the best experts on this subject based on the ideXlab platform.

  • Hyperbilirubinemia and kernicterus: 50 years later.
    Pediatrics, 2004
    Co-Authors: Joseph Lau, Mei Chung, John W. Kulig, Robert D. Sege, Stephan Glicken, Rebecca F. O'brien
    Abstract:

    In 1952, Hsia et al1 reported that 50% of infants with Erythroblastosis fetalis in whom the total serum bilirubin (TSB) was >30 mg/dL developed kernicterus. The authors further reported that kernicterus did not occur in >200 consecutive cases of Erythroblastosis fetalis when the hospital policy was to keep the serum bilirubin level

  • hyperbilirubinemia and kernicterus 50 years later
    Pediatrics, 2004
    Co-Authors: Joseph Lau, Mei Chung, John W. Kulig, Robert D. Sege, Stephan Glicken, Rebecca F Obrien
    Abstract:

    In 1952, Hsia et al1 reported that 50% of infants with Erythroblastosis fetalis in whom the total serum bilirubin (TSB) was >30 mg/dL developed kernicterus. The authors further reported that kernicterus did not occur in >200 consecutive cases of Erythroblastosis fetalis when the hospital policy was to keep the serum bilirubin level <20 mg/dL. They concluded that “although it has not been proved that bilirubin is the actual cause of brain damage, tests of serum bilirubin in infants with Erythroblastosis fetalis serve as extremely valuable guides to treatment.” There is no doubt that bilirubin plays a major role in the development of central nervous system pathology. High-quality studies2–7 …

Rebecca F Obrien - One of the best experts on this subject based on the ideXlab platform.

  • hyperbilirubinemia and kernicterus 50 years later
    Pediatrics, 2004
    Co-Authors: Joseph Lau, Mei Chung, John W. Kulig, Robert D. Sege, Stephan Glicken, Rebecca F Obrien
    Abstract:

    In 1952, Hsia et al1 reported that 50% of infants with Erythroblastosis fetalis in whom the total serum bilirubin (TSB) was >30 mg/dL developed kernicterus. The authors further reported that kernicterus did not occur in >200 consecutive cases of Erythroblastosis fetalis when the hospital policy was to keep the serum bilirubin level <20 mg/dL. They concluded that “although it has not been proved that bilirubin is the actual cause of brain damage, tests of serum bilirubin in infants with Erythroblastosis fetalis serve as extremely valuable guides to treatment.” There is no doubt that bilirubin plays a major role in the development of central nervous system pathology. High-quality studies2–7 …

Yukiko Komeno - One of the best experts on this subject based on the ideXlab platform.

  • Clinical Significance of Peripheral Blood Erythroblastosis after Hematopoietic Stem Cell Transplantation
    Leukemia & lymphoma, 2004
    Co-Authors: Susumu Goyama, Yoshinobu Kanda, Yasuhito Nannya, Seishi Ogawa, Yuki Asano-moki, Natsu Ogawa, Masahiro Nakagawa, Mamiko Sakata-yanagimoto, Masahito Kawazu, Yukiko Komeno
    Abstract:

    Erythroblasts (EBL) are normally not observed in peripheral blood, but may be found in patients suffering from a variety of severe diseases. The detection of EBL in peripheral blood has been shown to be associated with a poor prognosis. However, the clinical significance of peripheral Erythroblastosis after hematopoietic stem cell transplantation (HSCT) has not been evaluated. We retrospectively analyzed the records of 161 patients who underwent HSCT at our hospital from June 1995 to October 2001. EBL at any level were detected in 94% of the patients. Forty-four and 11 patients experienced Erythroblastosis exceeding 200 and 1,000/ul, respectively. The erythroblast count was higher in patients who died than in the survivors (geometric mean value 184 vs. 100/ul, P=0.01). High-level Erythroblastosis ( >1,000/ul) within 180 days after HSCT was associated with an extremely poor prognosis (median survival 22.5 days). Among the possible confounding factors, the use of total body irradiation (RR 2.35, 95% CI 1.22 - 4.54, P=0.011) and the disease status before transplantation (RR 2.51, 95% CI 1.15 - 5.49, P=0.021) were independent significant factors for Erythroblastosis after HSCT. As for post-transplant events, a high EBL concentration was frequently preceded by graft-vs.-host disease, thrombotic microangiopathy, hypoxia, and hematological relapse.

Ji Zhang - One of the best experts on this subject based on the ideXlab platform.

  • HEMATOPOIESIS Role of erythropoietin receptor signaling in Friend virus–induced Erythroblastosis and polycythemia
    2016
    Co-Authors: Ji Zhang, Melanie R. Loyd, Rachel L. Schweers, Derek A. Persons, Jerold E. Rehg, Constance T. Noguchi, James N. Ihle, Mindy S. R, Paul A. Ney
    Abstract:

    Friend virus is an acutely oncogenic retro-virus that causes Erythroblastosis and polycythemia in mice. Previous studies suggested that the Friend virus oncopro-tein, gp55, constitutively activates the erythropoietin receptor (EPOR), causing uncontrolled erythroid proliferation. Those studies showed that gp55 confers growth factor independence on an inter-leukin-3 (IL-3)–dependent cell line (Ba/F3) when the EPOR is coexpressed. Subse-quently, we showed that a truncated form of the stem-cell kinase receptor (sf-STK) is required for susceptibility to Friend disease. Given the requirement for sf-STK, we sought to establish the in vivo signifi-cance of gp55-mediated activation of the EPOR. We found that the cytoplasmic tyrosine residues of the EPOR, and signal transducer and activator of transcrip-tion-5 (STAT5), which acts through these sites, are not required for Friend virus– induced Erythroblastosis. The EPOR itself was required for the development of eryth-roblastosis but not for gp55-mediated ery-throid proliferation. Interestingly, the mu-rine EPOR, which is required for gp55-mediated Ba/F3-cell proliferation, was dispensable for Erythroblastosis in vivo. Finally, gp55-mediated activation of the EPOR and STAT5 are required for Friend virus–induced polycythemia. These results suggest that Friend virus activates both sf-STK and the EPOR to cause deregulated erythroid proliferation and differentiation

  • Role of erythropoietin receptor signaling in Friend virus-induced Erythroblastosis and polycythemia
    Blood, 2005
    Co-Authors: Ji Zhang, Mindy S. Randall, Melanie R. Loyd, Rachel L. Schweers, Derek A. Persons, Jerold E. Rehg, Constance T. Noguchi, James N. Ihle, Paul A. Ney
    Abstract:

    Friend virus is an acutely oncogenic retrovirus that causes Erythroblastosis and polycythemia in mice. Previous studies suggested that the Friend virus oncoprotein, gp55, constitutively activates the erythropoietin receptor (EPOR), causing uncontrolled erythroid proliferation. Those studies showed that gp55 confers growth factor independence on an interleukin-3 (IL-3)-dependent cell line (Ba/F3) when the EPOR is coexpressed. Subsequently, we showed that a truncated form of the stem-cell kinase receptor (sf-STK) is required for susceptibility to Friend disease. Given the requirement for sf-STK, we sought to establish the in vivo significance of gp55-mediated activation of the EPOR. We found that the cytoplasmic tyrosine residues of the EPOR, and signal transducer and activator of transcription-5 (STAT5), which acts through these sites, are not required for Friend virus-induced Erythroblastosis. The EPOR itself was required for the development of Erythroblastosis but not for gp55-mediated erythroid proliferation. Interestingly, the murine EPOR, which is required for gp55-mediated Ba/F3-cell proliferation, was dispensable for Erythroblastosis in vivo. Finally, gp55-mediated activation of the EPOR and STAT5 are required for Friend virus-induced polycythemia. These results suggest that Friend virus activates both sf-STK and the EPOR to cause deregulated erythroid proliferation and differentiation.