The DOI matches its Crossref record; 73 of the 73 references it cites were found in a registry or an index.
Mechanisms of Cardiac Dysfunction Associated With Tyrosine Kinase Inhibitor Cancer Therapeutics
Open accessAbstract
Treatment of patients with cancer has changed radically over the last several years with the advent of “targeted therapeutics.” Whereas traditional chemotherapy was directed at all rapidly dividing cells, whether cancerous or not, today’s anticancer drugs are increasingly tailored to the specific genetics of each cancer. This targeted approach, predominantly via inhibition of tyrosine kinase activity, has markedly improved the management of cancers including chronic myeloid leukemia (CML), breast cancer, gastrointestinal stromal tumor (GIST), renal cell carcinoma (RCC), and colon carcinoma.1–5 Inhibitors of tyrosine kinases are of 2 classes: monoclonal antibodies (mAbs), typically targeting growth factor receptor tyrosine kinases, and small molecules, referred to as tyrosine kinase inhibitors (TKIs), targeting both receptor and nonreceptor tyrosine kinases. The goal of targeted therapy is to improve antitumor activity with fewer toxic side effects than traditional anticancer therapies; given the initial success of this approach, the number of targeted therapy drugs entering into development in the last 5 years has increased dramatically.6,7 However, several recent studies have revealed unanticipated side effects of targeted therapy, including left ventricular (LV) dysfunction and heart failure, the primary manifestations of cardiotoxicity we will be examining here.5,8,9 Herein, we will examine the potential risk of LV dysfunction of targeted therapy and the molecular mechanisms that underlie that risk. We will review the importance of tyrosine kinase signaling pathways both for oncogenesis and for the survival of normal cardiomyocytes. To understand basic mechanisms of cardiomyopathy of TKIs, it is critical to understand 2 general classes of toxicity. The first is “on-target” toxicity, wherein the tyrosine kinase target regulating cancer cell survival and/or proliferation (and therefore a good target in cancer therapy) also serves an important role in normal cardiomyocyte survival, and thus inhibition leads to myocardial dysfunction. “Off-target” toxicity occurs when a TKI leads to toxicity …
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Cited by
Zamorano, J. L., Lancellotti, P., Rodriguez Muñoz, D., Aboyans, V., Asteggiano, R., Galderisi, M., Habib, G., Lenihan, D. J., Lip, G. Y. H., Lyon, A. R., et al. (2016) · European Heart Journal · doi:10.1093/eurheartj/ehw211 · Cited by 2,544
Advances in Therapeutic Interventions for Patients With Pulmonary Arterial Hypertension
Humbert, M., Lau, E. M. T., Montani, D., Jaïs, X., Sitbon, O., & Simonneau, G. (2014) · Circulation · doi:10.1161/circulationaha.114.006974 · Cited by 342
Akt Signaling in Macrophage Polarization, Survival, and Atherosclerosis
Linton, M. F., Moslehi, J. J., & Babaev, V. R. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20112703 · Cited by 285
De Angelis, A., Piegari, E., Cappetta, D., Marino, L., Filippelli, A., Berrino, L., Ferreira-Martins, J., Zheng, H., Hosoda, T., Rota, M., et al. (2010) · Circulation · doi:10.1161/circulationaha.109.895771 · Cited by 268
Cancer Therapy–Induced Cardiotoxicity: Basic Mechanisms and Potential Cardioprotective Therapies
Hahn, V. S., Lenihan, D. J., & Ky, B. (2014) · Journal of the American Heart Association · doi:10.1161/jaha.113.000665 · Cited by 264
Metadata
- Authors
- Chen, M. H., Kerkelä, R., & Force, T.
- Venue
- Circulation
- Published
- 2008-07
- Volume
- 118
- Issue
- 1
- Pages
- 84-95
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2157394282
- Cited by
- 379
- References
- 73
- FWCI
- 12.54
- Type
- journal article
- Language
- en
- Open access
- bronze
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