CXCR4-independent rescue of the myeloproliferative defect of the gata1low myelofibrosis mouse model by Aplidin

• Published in: Journal of cellular physiology Vol. 225; no. 2; pp. 490 - 499
• Main Authors: Verrucci, Maria, Pancrazzi, Alessandro, Aracil, Miguel, Martelli, Fabrizio, Guglielmelli, Paola, Zingariello, Maria, Ghinassi, Barbara, D'Amore, Emanuela, Jimeno, José, Vannucchi, Alessandro M., Migliaccio, Anna Rita
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.11.2010; Wiley Subscription Services, Inc
• Subjects: Age Distribution; Animals; Antineoplastic Agents - administration & dosage; Antineoplastic Agents - therapeutic use; Aplidin; Bone density; Bone growth; Bone Marrow Cells; Cell proliferation; Cells (biology); Clinical trials; CXCR4 protein; Cyclin-dependent kinase inhibitor p27; Cyclin-Dependent Kinase Inhibitor p27 - genetics; Cyclin-Dependent Kinase Inhibitor p27 - metabolism; Depsipeptides - administration & dosage; Depsipeptides - therapeutic use; Dose-Response Relationship, Drug; Drug Administration Schedule; Fibrosis; GATA-1 protein; GATA1 Transcription Factor - genetics; Gene Expression Regulation - drug effects; Hematopoiesis; Hematopoietic stem cells; Hemopoiesis; Hepatocytes; In vivo methods and tests; Janus kinase 2; Male; Megakaryocytes; Mice; Microenvironments; Mutation; Myelofibrosis; Neoplasms; Primary Myelofibrosis - genetics; Primary Myelofibrosis - metabolism; Progenitor cells; Receptors, CXCR4 - metabolism; Stem Cells - metabolism; Tumors; Vascular endothelial growth factor; Weight Loss - drug effects

The discovery of JAK2 mutations in Philadelphia‐negative myeloproliferative neoplasms has prompted investigators to evaluate mutation‐targeted treatments to restore hematopoietic cell functions in these diseases. However, the results of the first clinical trials with JAK2 inhibitors are not as promi...