Genomes and Genes
Affiliation: Stanford University
- JunB deficiency leads to a myeloproliferative disorder arising from hematopoietic stem cellsEmmanuelle 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...
- Hematopoietic stem cells, leukemic stem cells and chronic myelogenous leukemiaEmmanuelle 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...
- Global analysis of proliferation and cell cycle gene expression in the regulation of hematopoietic stem and progenitor cell fatesEmmanuelle 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....
- 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...
- Hematopoietic stem cell quiescence is maintained by compound contributions of the retinoblastoma gene familyPatrick 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...
- 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...
- New evidence supporting megakaryocyte-erythrocyte potential of flk2/flt3+ multipotent hematopoietic progenitorsE 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....
- Validation of MdmX as a therapeutic target for reactivating p53 in tumorsDaniel 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...
- Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switchSylvie 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...
- fester, A candidate allorecognition receptor from a primitive chordateSpencer 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...