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Interim positron emission tomography scans in diffuse large B-cell lymphoma: an independent expert nuclear medicine evaluation of the Eastern Cooperative Oncology Group E3404 study
VEGF/VEGFR2 interaction down-regulates matrix metalloproteinase–9 via STAT1 activation and inhibits B chronic lymphocytic leukemia cell migration
Issue Archive
January 28 2010
Table of Contents
INSIDE BLOOD
EDITORIALS
PLENARY PAPERS
REVIEW ARTICLES
CLINICAL TRIALS AND OBSERVATIONS
Interim positron emission tomography scans in diffuse large B-cell lymphoma: an independent expert nuclear medicine evaluation of the Eastern Cooperative Oncology Group E3404 study
CME
Sandra J. Horning,Malik E. Juweid,Heiko Schöder,Gregory Wiseman,Alex McMillan,Lode J. Swinnen,Ranjana Advani,Randy Gascoyne,Andrew Quon
GENE THERAPY
HEMATOPOIESIS AND STEM CELLS
IMMUNOBIOLOGY
Rap1 controls lymphocyte adhesion cascade and interstitial migration within lymph nodes in RAPL-dependent and -independent manners
Yukihiko Ebisuno,Koko Katagiri,Tomoya Katakai,Yoshihiro Ueda,Tomomi Nemoto,Hiroyuki Inada,Junichi Nabekura,Takaharu Okada,Reiji Kannagi,Toshiyuki Tanaka,Masayuki Miyasaka,Nancy Hogg,Tatsuo Kinashi
LYMPHOID NEOPLASIA
VEGF/VEGFR2 interaction down-regulates matrix metalloproteinase–9 via STAT1 activation and inhibits B chronic lymphocytic leukemia cell migration
Brief Report
Estefanía Ugarte-Berzal,Javier Redondo-Muñoz,Pilar Eroles,Mercedes Hernández del Cerro,José A. García-Marco,María José Terol,Angeles García-Pardo
RED CELLS, IRON, AND ERYTHROPOIESIS
THROMBOSIS AND HEMOSTASIS
VASCULAR BIOLOGY
CORRESPONDENCE
G-CSF–induced aneuploidy does not affect CD34+ cells and does not require cell division
Caroline Marmier-Savet,Fabrice Larosa,Faezeh Legrand,Brigitte Witz,Mauricette Michallet,Dana Ranta,Pascale Louvat,Marc Puyraveau,Nicole Raus,Maribel Tavernier,Suzanne Mathieu-Nafissi,Olivier Hequet,Jean-René Pallandre,Franck Vitte,Marie-Agnès Collonge-Rame,Fabienne Pouthier,Jean-Luc Bresson,Eric Deconinck,Pierre Tiberghien,Eric Robinet
OTHER DEPARTMENTS
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Cover Image
Cover Image
Hypothetical schema for the effects of the tyrosine kinase inhibitor imatinib on bone metabolism. Imatinib causes increased bone volume by inhibiting osteoclast (OC) formation and activity and increasing osteoblast (OB) activity. The inhibitory effects of imatinib on signaling through c-fms and, potentially, c-kit, CAII, and PDGFR decreases the formation and activity of bone-resorbing OC. Additionally, inhibition of PDGFR by imatinib inhibits OB proliferation but also relieves the inhibitory effects of PDGF on OB bone formation. See the article by Vandyke et al on page 766.
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