Dark Side of Cancer Therapy: Cancer Treatment-Induced Cardiopulmonary Inflammation, Fibrosis, and Immune Modulation

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.

The Association of Blood Urea Nitrogen to Creatinine Ratio and the Prognosis of Critically Ill Patients with Cerebral Infarction: A Cohort Study

“…In this study, the association between BUN/Cr and the increased risk of in-hospital mortality of cerebral infarction patients was observed in subgroups including males and those with respiratory failure, malignant cancer, and without liver disease, as well as those receiving anticoagulation. Patients with respiratory failure and malignant cancer might be associated with a higher infection and inflammation status [ 29 , 30 ]. Anticoagulation was applied for the treatment of venous thrombosis and prophylaxis of postoperative venous thrombosis [ 31 ].…”

Cuproptosis-related gene DLAT is a prognostic and immunological biomarker in pan-cancer

“…According to statistics, there were about 19.3 million new cancer cases and 10 million deaths worldwide in 2020 (Sung et al 2021). Although the emergence of various targeted therapies, some cancer patients still have poor therapeutic effects due to the complexity of tumor mechanisms (Boopathi and Thangavel 2021). Therefore, searching for valuable pan-cancer genes is of great importance to elucidate the pathogenesis of different cancers.…”

Tumor accomplice: T cell exhaustion induced by chronic inflammation

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