Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Apr;24(4):475-491.
doi: 10.1007/s11912-022-01215-1. Epub 2022 Feb 22.

Cardiovascular Risks with Epidermal Growth Factor Receptor (EGFR) Tyrosine Kinase Inhibitors and Monoclonal Antibody Therapy

Kalyan R Chitturi  1 , Ethan A Burns  2 , Ibrahim N Muhsen  3 , Kartik Anand  4 , Barry H Trachtenberg  5
Affiliations
Review

Cardiovascular Risks with Epidermal Growth Factor Receptor (EGFR) Tyrosine Kinase Inhibitors and Monoclonal Antibody Therapy

Kalyan R Chitturi et al. Curr Oncol Rep. 2022 Apr.

Abstract

Purpose of review: Tyrosine kinase inhibitors (TKI) and monoclonal antibodies (mAbs) that target the epidermal growth factor receptor (EGFR) have changed the therapeutic landscape across a range of solid malignancies. However, there is little data regarding the cardiovascular (CV) impact of these agents. The purpose of this review is to discuss reported CV effects, pathophysiology, pre-treatment screening, diagnostic workup, and treatment recommendations in this patient population.

Recent findings: It is apparent that CV events are not class dependent, and while infrequently reported in clinical trials, unique CV toxicity may occur with EGFR inhibitors, including structural, electrical, and vascular events. There remains an unmet need to fully elucidate the spectrum of CV events associated with EGFR inhibitors. Early CV screening, close clinical monitoring, coupled with a multidisciplinary approach between medical and cardio-oncology is needed to minimize the potentially detrimental impact of cardiotoxicity in this patient population.

Keywords: Cancer; Cardio-oncology; Cardiovascular toxicity; EGFR mutation; Monoclonal antibody; Tyrosine kinase inhibitor.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance
    1. Chen MH, Kerkelä R, Force T. Mechanisms of cardiac dysfunction associated with tyrosine kinase inhibitor cancer therapeutics. Circulation. 2008;118(1):84–95. https://doi.org/10.1161/CIRCULATIONAHA.108.776831 . - DOI - PubMed - PMC
    1. Holbro T, Hynes NE. ErbB receptors: directing key signaling networks throughout life. Annu Rev Pharmacol Toxicol. 2004;44:195–217. https://doi.org/10.1146/annurev.pharmtox.44.101802.121440 . - DOI - PubMed
    1. Hervent AS, De Keulenaer GW. Molecular mechanisms of cardiotoxicity induced by ErbB receptor inhibitor cancer therapeutics. Int J Mol Sci. 2012;13(10):12268–86. https://doi.org/10.3390/ijms131012268 . - DOI - PubMed - PMC
    1. Yarden Y, Sliwkowski MX. Untangling the ErbB signalling network. Nat Rev Mol Cell Biol. 2001;2(2):127–37. https://doi.org/10.1038/35052073 . - DOI - PubMed
    1. Ozcelik C, Erdmann B, Pilz B, et al. Conditional mutation of the ErbB2 (HER2) receptor in cardiomyocytes leads to dilated cardiomyopathy. Proc Natl Acad Sci U S A. 2002;99(13):8880–5. https://doi.org/10.1073/pnas.122249299 . - DOI - PubMed - PMC

MeSH terms

LinkOut - more resources