Emmanuelle Passegue

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. ncbi JunB deficiency leads to a myeloproliferative disorder arising from hematopoietic stem cells
    Emmanuelle Passegue
    Institute of Cancer and Stem Cell Biology and Medicine, Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cell 119:431-43. 2004
  2. ncbi Hematopoietic stem cells, leukemic stem cells and chronic myelogenous leukemia
    Emmanuelle Passegue
    Department of Pathology, StanfordUniversity School of Medicine, Beckman Center, California 94305, USA
    Cell Cycle 4:266-8. 2005
  3. ncbi Global analysis of proliferation and cell cycle gene expression in the regulation of hematopoietic stem and progenitor cell fates
    Emmanuelle Passegue
    Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Exp Med 202:1599-611. 2005
  4. ncbi Leukemic stem cells: where do they come from?
    Emmanuelle Passegue
    Stanford University School of Medicine, Pathology Department, Beckman Center B259, Stanford, CA 94305, USA
    Stem Cell Rev 1:181-8. 2005
  5. ncbi Hematopoietic stem cell quiescence is maintained by compound contributions of the retinoblastoma gene family
    Patrick Viatour
    Department of Pediatrics, Stanford Medical School, Stanford, CA 94305, USA
    Cell Stem Cell 3:416-28. 2008
  6. ncbi Normal and leukemic hematopoiesis: are leukemias a stem cell disorder or a reacquisition of stem cell characteristics?
    Emmanuelle Passegue
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 100:11842-9. 2003
  7. ncbi New evidence supporting megakaryocyte-erythrocyte potential of flk2/flt3+ multipotent hematopoietic progenitors
    E Camilla Forsberg
    Institute of Stem Cell Biology and Regenerative Medicine, Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cell 126:415-26. 2006
  8. ncbi Validation of MdmX as a therapeutic target for reactivating p53 in tumors
    Daniel Garcia
    Department of Pathology, UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, California 94143, USA
    Genes Dev 25:1746-57. 2011
  9. ncbi Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switch
    Sylvie Giuriato
    Departments of Medicine and Pathology, Division of Oncology, Stanford University School of Medicine, CCSR Building, Room 1120, 269 Campus Drive, Stanford, CA 94305 5151, USA
    Proc Natl Acad Sci U S A 103:16266-71. 2006
  10. ncbi fester, A candidate allorecognition receptor from a primitive chordate
    Spencer V Nyholm
    Department of Pathology, Stanford University School of Medicine, California 94305, USA
    Immunity 25:163-73. 2006

Collaborators

Detail Information

Publications10

  1. ncbi JunB deficiency leads to a myeloproliferative disorder arising from hematopoietic stem cells
    Emmanuelle Passegue
    Institute of Cancer and Stem Cell Biology and Medicine, Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cell 119:431-43. 2004
    ..These results demonstrate a stem cell-specific role for JunB in normal and leukemic hematopoiesis and provide experimental evidence that leukemic stem cells (LSC) can reside at the LT-HSC stage of development in a mouse model of MPD...
  2. ncbi Hematopoietic stem cells, leukemic stem cells and chronic myelogenous leukemia
    Emmanuelle Passegue
    Department of Pathology, StanfordUniversity School of Medicine, Beckman Center, California 94305, USA
    Cell Cycle 4:266-8. 2005
    ..Given the clinical importance of LSC identification, the insights gained through these approaches will quickly translate into clinical applications and lead to improved treatments for human leukemias...
  3. ncbi Global analysis of proliferation and cell cycle gene expression in the regulation of hematopoietic stem and progenitor cell fates
    Emmanuelle Passegue
    Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Exp Med 202:1599-611. 2005
    ....
  4. ncbi Leukemic stem cells: where do they come from?
    Emmanuelle Passegue
    Stanford University School of Medicine, Pathology Department, Beckman Center B259, Stanford, CA 94305, USA
    Stem Cell Rev 1:181-8. 2005
    ..Such approaches in the mouse are essential for the basic understanding of leukemogenesis and for the conceptual design of novel therapeutic strategies that could lead to improved treatments for human leukemias...
  5. ncbi Hematopoietic stem cell quiescence is maintained by compound contributions of the retinoblastoma gene family
    Patrick Viatour
    Department of Pediatrics, Stanford Medical School, Stanford, CA 94305, USA
    Cell Stem Cell 3:416-28. 2008
    ..The presence of a single p107 allele is sufficient to largely rescue these defects. Thus, Rb family members collectively maintain HSC quiescence and the balance between lymphoid and myeloid cell fates in the hematopoietic system...
  6. ncbi Normal and leukemic hematopoiesis: are leukemias a stem cell disorder or a reacquisition of stem cell characteristics?
    Emmanuelle Passegue
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 100:11842-9. 2003
    ..Moreover, LSC identification and purification will provide a powerful diagnostic, prognostic, and therapeutic tool in the clinic...
  7. ncbi New evidence supporting megakaryocyte-erythrocyte potential of flk2/flt3+ multipotent hematopoietic progenitors
    E Camilla Forsberg
    Institute of Stem Cell Biology and Regenerative Medicine, Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cell 126:415-26. 2006
    ....
  8. ncbi Validation of MdmX as a therapeutic target for reactivating p53 in tumors
    Daniel Garcia
    Department of Pathology, UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, California 94143, USA
    Genes Dev 25:1746-57. 2011
    ..Hence, systemic inhibition of MdmX is both a feasible therapeutic strategy for restoring p53 function in tumors that retain wild-type p53 and likely to be significantly safer than inhibition of Mdm2...
  9. ncbi Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switch
    Sylvie Giuriato
    Departments of Medicine and Pathology, Division of Oncology, Stanford University School of Medicine, CCSR Building, Room 1120, 269 Campus Drive, Stanford, CA 94305 5151, USA
    Proc Natl Acad Sci U S A 103:16266-71. 2006
    ..Therefore, the combined inactivation of oncogenes and angiogenesis may be a more clinically effective treatment of cancer. We conclude that angiogenesis is an essential component of oncogene addiction...
  10. ncbi fester, A candidate allorecognition receptor from a primitive chordate
    Spencer V Nyholm
    Department of Pathology, Stanford University School of Medicine, California 94305, USA
    Immunity 25:163-73. 2006
    ..The genetic and somatic diversity, coupled to the expression and functional data, suggests that fester is a receptor involved in histocompatibility...