(Circulation. 2002;106:e220.)
© 2002 American Heart Association, Inc.
Correspondence |
Biomedical Research Consultants, 2821 North Course Dr (H-205), Pompano Beach, FL 33069
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
To the Editor:
Grines et al1 assert that the vascular endothelium and/or the myocardium can incorporate a human, replication-deficient adenovirus vector (Ad5-FGF4) in which one gene is replaced with the human FGF4 gene that is delivered by intracoronary infusion. This, according to the authors, allows sustained in situ production of "angiogenic growth factors." The data show, however, that the vector was detected in the pulmonary artery and later in the venous blood. Thus, the alleged lack of systemic exposure to the unidentified growth factors is not convincing.
The observation that 2 patients (3%) were diagnosed with malignancies 69 days (brain) and 267 days (colon) after the treatment was dismissed as unrelated occurrences. Furthermore, the report does not discuss the more general angiogenesis-neoplasia link, described initially nearly 100 years ago. In 1971, Folkman advanced the now well accepted postulate that tumor growth and metastasis are angiogenesis-dependent, and hence blocking angiogenesis could be an effective strategy to arrest tumor proliferation.2 Not surprisingly, in 2000, the journal Cancer and Metastasis Review published nearly 200 pages of contributions on the angiogenesis-neoplasia association.3 In addition, neovascularization of untargeted tissues may initiate or aggravate other pathological states with serious clinical consequences, such as rheumatoid arthritis, retinopathies (including macular degeneration), psoriasis, and hemangiomas. In a critical essay, Epstein et al4 emphasized the still overlooked serious side effects resulting from administration of angiogenic agents and concluded explicitly, "We are not seduced by hype and we judge the merits of this potential important and novel therapeutic approach to obstructive arterial disease in
Director, Cardiac Catheterization Laboratories, William Beaumont Hospital, Cardiology Administration/3rd Floor, 3601 West Thirteen Mile Rd, Royal Oak, MI 48073-6769
President and Chairman, Collateral Therapeutics, San Diego, Calif
Johns Hopkins Hospital, Baltimore, Md
Minnesota Heart Clinic, Minneapolis, Minn
Mount Sinai Medical Center, New York, NY
UCSD San Diego VA Medical Center, San Diego, Calif
Fletcher Allen Health Center, Burlington, Vt
Berlex Laboratories, Inc, Montville, NJ
Professor of Medicine, VA San Diego, San Diego, Calif
Heart and Vascular Institute of Texas, San Antonio, Tex
This article has been cited by other articles:
![]() |
Y. Wang, X. Wei, X. Xiao, R. Hui, J. W. Card, M. A. Carey, D. W. Wang, and D. C. Zeldin Arachidonic Acid Epoxygenase Metabolites Stimulate Endothelial Cell Growth and Angiogenesis via Mitogen-Activated Protein Kinase and Phosphatidylinositol 3-Kinase/Akt Signaling Pathways J. Pharmacol. Exp. Ther., August 1, 2005; 314(2): 522 - 532. [Abstract] [Full Text] [PDF] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2002 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |