Abstract
Advancements in cancer therapy increased the cancer free survival rates and reduced the malignant related deaths. Therapeutic options for patients with thoracic cancers include surgical intervention and the application of chemotherapy with ionizing radiation. Despite these advances, cancer therapy-related cardiopulmonary dysfunction (CTRCPD) is one of the most undesirable side effects of cancer therapy and leads to limitations to cancer treatment. Chemoradiation therapy or immunotherapy promote acute and chronic cardiopulmonary damage by inducing reactive oxygen species, DNA damage, inflammation, fibrosis, deregulation of cellular immunity, cardiopulmonary failure, and non-malignant related deaths among cancer-free patients who received cancer therapy. CTRCPD is a complex entity with multiple factors involved in this pathogenesis. Although the mechanisms of cancer therapy-induced toxicities are multifactorial, damage to the cardiac and pulmonary tissue as well as subsequent fibrosis and organ failure seem to be the underlying events. The available biomarkers and treatment options are not sufficient and efficient to detect cancer therapy-induced early asymptomatic cell fate cardiopulmonary toxicity. Therefore, application of cutting-edge multi-omics technology, such us whole-exome sequencing, DNA methylation, whole-genome sequencing, metabolomics, protein mass spectrometry and single cell transcriptomics, and 10 X spatial genomics, are warranted to identify early and late toxicity, inflammation-induced carcinogenesis response biomarkers, and cancer relapse response biomarkers. In this review, we summarize the current state of knowledge on cancer therapy-induced cardiopulmonary complications and our current understanding of the pathological and molecular consequences of cancer therapy-induced cardiopulmonary fibrosis, inflammation, immune suppression, and tumor recurrence, and possible treatment options for cancer therapy-induced cardiopulmonary toxicity.
Highlights
Thoracic cancers include thymic and windpipe cancers, breast cancerinduced lung metastasis, and non-small cell lung cancers (NSCLCs) as the most common [1]
Treatment options depend on the stage and type of cancer, which includes surgical removal of cancer tissue followed by chemotherapy or radiation, or a combination of chemoradiation therapy (CRT) and immunotherapy
We summarize the current state of knowledge on the cardiopulmonary complications of cancer therapy and our current understanding of the pathological and molecular consequences of cancer therapy-induced cardiopulmonary toxicity, as well as the relationship between chronic inflammation and cancer
Summary
Thoracic cancers include thymic and windpipe (tracheal) cancers, breast cancerinduced lung metastasis, and non-small cell lung cancers (NSCLCs) as the most common [1]. Radiation therapy promotes immune suppression via immune modulator programmed death ligand-1 (PD-L1) in cancer patients. These toxicities lead to cardiac myopathy, hypertension, myocarditis, left ventricular dysfunction, ventricular arrhythmias, pulmonary edema, pulmonary hemorrhage, and pulmonary pneumonitis [5,11,12,13,14,15,16,17,18,19,20,21,22]. Different ways by which cancer therapy promotes lung and heart toxicity include 1) cancer therapy-induced cardiopulmonary inflammation and fibrosis, and 2) cancer therapy (radiation therapy)-induced immune suppression. We discuss the possible treatment options and management of cancer therapy-induced cardiopulmonary toxicity and chronic inflammation
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