Molecularly targeted anti-cancer therapies have revolutionized cancer treatment by improving both quality of life and survival in cancer patients. However, many of these drugs are associated with cardiovascular toxicities that are sometimes dose-limiting. Moreover, the long-term cardiovascular consequences of these drugs, some of which are used chronically, are not yet known. Although the scope and mechanisms of the cardiac toxicities are better defined, the mechanisms for vascular toxicities are only beginning to be elucidated. This review summarizes what is known about the vascular adverse events associated with three classes of novel anti-cancer therapies: vascular endothelial growth factor (VEGF) inhibitors, breakpoint cluster-Abelson (BCR-ABL) kinase inhibitors used to treat chronic myelogenous leukaemia (CML) and immunomodulatory agents (IMiDs) used in myeloma therapeutics. Three of the best described vascular toxicities are reviewed including hypertension, increased risk of acute cardiovascular ischaemic events and arteriovenous thrombosis. The available data regarding the mechanism by which each therapy causes vascular complication are summarized. When data are limited, potential mechanisms are inferred from the known effects of inhibiting each target on vascular cell function and disease. Enhanced understanding of the molecular mechanisms of vascular side effects of targeted cancer therapy is necessary to effectively manage cancer patients and to design safer targeted cancer therapies for the future.
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October 2016
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Targeted cancer treatment. In this issue, Gopal et al, review the molecular mechanisms of vascular complications of targeted cancer therapies. See pp. 1763–1779 for further details.
Review Article|
September 09 2016
Molecular mechanisms for vascular complications of targeted cancer therapies
Srila Gopal;
*Department of Medicine, Division of Hematology/Oncology, Tufts Medical Center, Boston, MA 02111, U.S.A.
†Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02111, U.S.A.
Correspondence: Dr Srila Gopal (email srilagopal@gmail.com) or Dr Iris Zamir Jaffe (email ijaffe@tuftsmedicalcenter.org)
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Kenneth B. Miller;
Kenneth B. Miller
*Department of Medicine, Division of Hematology/Oncology, Tufts Medical Center, Boston, MA 02111, U.S.A.
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Iris Z. Jaffe
†Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA 02111, U.S.A.
‡Department of Medicine, Division of Cardiology, Tufts Medical Center, Boston, MA 02111, U.S.A.
Correspondence: Dr Srila Gopal (email srilagopal@gmail.com) or Dr Iris Zamir Jaffe (email ijaffe@tuftsmedicalcenter.org)
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Publisher: Portland Press Ltd
Received:
March 31 2016
Revision Received:
July 12 2016
Accepted:
July 22 2016
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2016 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society
2016
Clin Sci (Lond) (2016) 130 (20): 1763–1779.
Article history
Received:
March 31 2016
Revision Received:
July 12 2016
Accepted:
July 22 2016
Citation
Srila Gopal, Kenneth B. Miller, Iris Z. Jaffe; Molecular mechanisms for vascular complications of targeted cancer therapies. Clin Sci (Lond) 1 October 2016; 130 (20): 1763–1779. doi: https://doi.org/10.1042/CS20160246
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