Emmanuelle Passegue

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. pmc 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
  2. ncbi request reprint 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
  3. ncbi request reprint 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
  4. ncbi request reprint 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
  5. pmc Similar MLL-associated leukemias arising from self-renewing stem cells and short-lived myeloid progenitors
    Antonio Cozzio
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Genes Dev 17:3029-35. 2003
  6. pmc 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
  7. ncbi request reprint MLL-GAS7 transforms multipotent hematopoietic progenitors and induces mixed lineage leukemias in mice
    Chi Wai So
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cancer Cell 3:161-71. 2003
  8. pmc 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
  9. ncbi request reprint Chronic versus acute myelogenous leukemia: a question of self-renewal
    Catriona H M Jamieson
    Institute of Cancer and Stem Cell Biology and Medicine, Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cancer Cell 6:531-3. 2004
  10. ncbi request reprint 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

Collaborators

Detail Information

Publications13

  1. pmc 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
    ....
  2. ncbi request reprint 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...
  3. ncbi request reprint 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...
  4. ncbi request reprint 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...
  5. pmc Similar MLL-associated leukemias arising from self-renewing stem cells and short-lived myeloid progenitors
    Antonio Cozzio
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Genes Dev 17:3029-35. 2003
    ....
  6. pmc 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...
  7. ncbi request reprint MLL-GAS7 transforms multipotent hematopoietic progenitors and induces mixed lineage leukemias in mice
    Chi Wai So
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cancer Cell 3:161-71. 2003
    ..This experimental modeling of ABL in mice highlights its origin from multipotential progenitors that arrest at a bipotential stage specifically targeted or induced by MLL oncogenes...
  8. pmc 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...
  9. ncbi request reprint Chronic versus acute myelogenous leukemia: a question of self-renewal
    Catriona H M Jamieson
    Institute of Cancer and Stem Cell Biology and Medicine, Departments of Pathology and Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cancer Cell 6:531-3. 2004
    ....
  10. ncbi request reprint 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
    ....
  11. pmc 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...
  12. pmc 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...
  13. ncbi request reprint 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...