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 Blood, 15 October 2008, Vol. 112, No. 8, pp. 3026-3035.
Prepublished online as a Blood First Edition Paper on July 31, 2008; DOI 10.1182/blood-2008-06-158386.

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REVIEW ARTICLES

Does primary myelofibrosis involve a defective stem cell niche? From concept to evidence

Jean-Jacques Lataillade1, Olivier Pierre-Louis2,3, Hans Carl Hasselbalch4, Georges Uzan2,3, Claude Jasmin2,3, Marie-Claire Martyré2,3, Marie-Caroline Le Bousse-Kerdilès2,3, on behalf of the French INSERM and the European EUMNET Networks on Myelofibrosis

1 Laboratoire de Recherche, Center de Transfusion Sanguine des Armeés (CTSA), Hôpital Percy, Clamart, France; 2 INSERM U602, Hôpital Paul Brousse, Villejuif, France; 3 Université Paris 11, Institut Fédératif de Recherche (IFR) 89, Institut André Lwoff, Villejuif, France; and 4 Department of Hematology, Herlev University Hospital, Copenhagen, Denmark

Primary myelofibrosis (PMF) is the rarest and the most severe Philadelphia-negative chronic myeloproliferative syndrome. By associating a clonal proliferation and a mobilization of hematopoietic stem cells from bone marrow to spleen with profound alterations of the stroma, PMF is a remarkable model in which deregulation of the stem cell niche is of utmost importance for the disease development. This paper reviews key data suggesting that an imbalance between endosteal and vascular niches participates in the development of clonal stem cell proliferation. Mechanisms by which bone marrow niches are altered with ensuing mobilization and homing of neoplastic hematopoietic stem cells in new or reinitialized niches in the spleen and liver are examined. Differences between signals delivered by both endosteal and vascular niches in the bone marrow and spleen of patients as well as the responsiveness of PMF stem cells to their specific signals are discussed. A proposal for integrating a potential role for the JAK2 mutation in their altered sensitivity is made. A better understanding of the cross talk between stem cells and their niche should imply new therapeutic strategies targeting not only intrinsic defects in stem cell signaling but also regulatory hematopoietic niche–derived signals and, consequently, stem cell proliferation.


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