| HOME | HELP | CONTACT US | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
M.D. Anderson Cancer Center, Houston, Texas, USA
Correspondence: Francis J. Giles, M.D., Chief, Section of Developmental Therapeutics, Associate Professor of Medicine, Department of Leukemia, MD Anderson Cancer Center, 1515 Holcombe Boulevard, Box 428, Houston, Texas 77030, USA. Telephone: 713-792-8217; Fax: 713-794-4297; e-mail: fgiles{at}mdanderson.org
Angiogenesis is an important component in the progression and metastasis of solid tumors. We now appreciate that angiogenesis is also critically involved in the pathogenesis of hematologic malignancies. Current data suggest important prognostic and therapeutic implications of angiogenesis in a variety of malignancies of the hematopoietic system, including acute and chronic leukemias, myeloproliferative diseases, multiple myeloma, non-Hodgkin's lymphomas, and Hodgkin's disease. Vascular endothelial growth factor (VEGF) is a major angiogenic factor that regulates multiple endothelial cell functions, including mitogenesis. Cellular and circulating levels of VEGF are elevated in hematologic malignancies and are adversely associated with prognosis. Angiogenesis is a very complex, tightly regulated, multistep process, the targeting of which may well prove useful in the creation of novel therapeutic agents. Current approaches being investigated include the inhibition of angiogenesis stimulants (e.g., VEGF), or their receptors, blockade of endothelial cell activation, inhibition of matrix metalloproteinases, and inhibition of tumor vasculature. Preclinical, phase I, and phase II studies of both monoclonal antibodies to VEGF and blockers of the VEGF receptor tyrosine kinase pathway indicate that these agents are safe and offer potential clinical utility in patients with hematologic malignancies.
This article has been cited by other articles:
![]() |
G. W. Prager, J. M. Breuss, S. Steurer, J. Mihaly, and B. R. Binder Vascular endothelial growth factor (VEGF) induces rapid prourokinase (pro-uPA) activation on the surface of endothelial cells Blood, February 1, 2004; 103(3): 955 - 962. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. J. Lukiw, A. Ottlecz, G. Lambrou, M. Grueninger, J. Finley, H. W. Thompson, and N. G. Bazan Coordinate Activation of HIF-1 and NF-{kappa}B DNA Binding and COX-2 and VEGF Expression in Retinal Cells by Hypoxia Invest. Ophthalmol. Vis. Sci., October 1, 2003; 44(10): 4163 - 4170. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. J. Giles, A. T. Stopeck, L. R. Silverman, J. E. Lancet, M. A. Cooper, A. L. Hannah, J. M. Cherrington, A.-M. O'Farrell, H. A. Yuen, S. G. Louie, et al. SU5416, a small molecule tyrosine kinase receptor inhibitor, has biologic activity in patients with refractory acute myeloid leukemia or myelodysplastic syndromes Blood, August 1, 2003; 102(3): 795 - 801. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. J. Giles, A. Keating, A. H. Goldstone, I. Avivi, C. L. Willman, and H. M. Kantarjian Acute Myeloid Leukemia Hematology, January 1, 2002; 2002(1): 73 - 110. [Abstract] [Full Text] |
||||
![]() |
J. L. Gabrilove Hematologic Malignancies: An Opportunity for Targeted Drug Therapy Oncologist, October 1, 2001; 6(2008): 1 - 3. [Full Text] [PDF] |
||||
![]() |
J. L. Gabrilove Angiogenic Growth Factors: Autocrine and Paracrine Regulation of Survival in Hematologic Malignancies Oncologist, October 1, 2001; 6(2008): 4 - 7. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | CONTACT US | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| THE ONCOLOGIST | STEM CELLS | CME | ALPHAMED PRESS JOURNALS |