Cancer therapy-associated cardiotoxicity and signaling in the myocardium

Zuppinger, Christian; Suter, Thomas M (2010). Cancer therapy-associated cardiotoxicity and signaling in the myocardium. Journal of cardiovascular pharmacology, 56(2), pp. 141-6. Hagerstown, Md.: Wolters Kluwer Lippincott Williams & Wilkins 10.1097/FJC.0b013e3181e0f89a

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The cardiotoxic potential of cytotoxic cancer chemotherapy is well known. Prime examples are the anthracyclines, which are highly efficacious agents for hemopoietic malignancies and solid tumors, but their clinical use is limited primarily by cardiotoxicity. Besides the conventional chemotherapeutics, new cancer drugs were developed in the last decade with the goal to specifically inhibit selected molecular targets such as growth factor receptors or intracellular tyrosine kinases in cancer cells. However, the outcome of combining conventional and newer cancer therapies could have unexpected side effects not anticipated so far and the long-term outcome is not known. Sometimes, however, unexpected side effects also shed light on previously unknown physiological functions. For example, the anti-HER2 cancer therapeutic trastuzumab (Herceptin), which can induce cardiac dysfunction, has demonstrated the importance of the ErbB/neuregulin signaling system in the adult heart. Subsequently, the role of endothelial-myocardial communication in maintaining phenotype and survival of adult cardiomyocytes has increasingly been recognized.

Item Type:

Journal Article (Further Contribution)

Division/Institute:

04 Faculty of Medicine > Department of Cardiovascular Disorders (DHGE) > Clinic of Cardiology

UniBE Contributor:

Zuppinger, Christian, Suter, Thomas

ISSN:

0160-2446

Publisher:

Wolters Kluwer Lippincott Williams & Wilkins

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:10

Last Modified:

05 Dec 2022 14:01

Publisher DOI:

10.1097/FJC.0b013e3181e0f89a

PubMed ID:

20386457

Web of Science ID:

000281123300004

URI:

https://boris.unibe.ch/id/eprint/1616 (FactScience: 203394)

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