From Bench to Bedside: Translational Approaches to Cardiotoxicity in Breast Cancer, Lung Cancer, and Lymphoma Therapies

Abstract

Cardiotoxicity represents a critical challenge in cancer therapy, particularly in the treatment of thoracic tumors, such as lung cancer and lymphomas, as well as breast cancer. These malignancies stand out for their high prevalence and the widespread use of cardiotoxic treatments, such as chemotherapy, radiotherapy, and immunotherapy. This work underscores the importance of preclinical models in uncovering the mechanisms of cardiotoxicity and developing targeted prevention and mitigation strategies. In vitro models provide valuable insights into cellular processes, enabling the observation of changes in cell viability and function following exposure to various drugs or ionizing radiation. Complementarily, in vivo animal models offer a broader perspective, allowing for evaluating of both short- and long-term effects and a better understanding of chronic toxicity and cardiac diseases. By integrating these approaches, researchers can identify potential mechanisms of cardiotoxicity and devise effective prevention strategies. This analysis highlights the central role of preclinical models in advancing knowledge of cardiotoxic effects associated with common therapeutic regimens for thoracic and breast cancers.

Keywords: cardiotoxicity; chemotherapy; immunotherapy; preclinical models; radiotherapy.

Figure 1

Anti-cancer treatments’ side effects on heart.

Figure 2

Research models for the evaluation of cardiotoxicity induced by anti-cancer treatments.

Figure 3

Pathway illustrating the progression from radiation-induced epithelial/endothelial damage to fibroatrophy via inflammation, fibroblast activation, ECM remodeling, and tissue atrophy.

Figure 4

Diagram illustrating the development of ICI-associated myocarditis. Under naïve conditions, PD-1/PD-L1 interactions prevent T cell activation, avoiding myocarditis. With ICI treatment (anti-PD-1 mAb), cardiac myosin-specific T cells are activated, releasing IFN-γ, perforin, and granzyme B, leading to immune-mediated myocarditis.