Cross-disease communication between cancer and heart failure provides a rational approach to prevention and treatment of both diseases

Abstract

Accumulating clinical data have demonstrated a clear positive association between cancer and cardiac disorders, particularly chronic heart failure (CHF). These two diseases can be mutual drivers of each other, and hence frequently co-occur in patients. The immune system is the core mechanism that eliminates transformed cells from our bodies. However, immune cells often play distinct or even conflicting roles in cancer and CHF. Moreover, CHF alters the properties of immune cells, particularly those of regulatory T cells. Our previous study showed that the oxidative phosphorylation capacity of peripheral blood mononuclear cells is impaired in CHF, leading to the increased production of reactive oxygen species. Therefore, the co-occurrence of cancer and CHF becomes a serious problem, affecting the treatment of both diseases, and consequently negatively affecting patient survival rates. To date, few methods have been identified that effectively treat both diseases at the same time. Mitochondria activity may change in immune cells during their activation and exhaustion, and in CHF. Mitochondria activity is also largely affected in myocardia in CHF. We here focus on the mitochondrial abnormalities of immune cells in cancer and CHF, and discuss possible ways to treat cancer and CHF at the same time by targeting mitochondrial abnormalities. Many cancer cells are inevitably produced daily in our bodies, mostly owing to enzymatic nucleotide errors of DNA replication and repair. Therefore, the possibility of ways to prevent cancer by preventing the onset of heart failure will also be discussed.

KRAS, MYC, and ARF6: inseparable relationships cooperatively promote cancer malignancy and immune evasion

“…Immunity is essential not only in immunotherapy but also in chemotherapy-based cancer treatments [ 67 ]. Thus, as we have discussed recently [ 68 ], improving circulatory problems might be a prerequisite for effective cancer therapeutics in many cases, including those targeting KRAS and G4.…”

Mitochondrial dysfunction at the crossroad of cardiovascular diseases and cancer

“…Furthermore, the same genetic and cellular mechanisms could play a pathogenic role in both CVDs and cancer, including inflammatory signalling, reactive oxygen species (ROS), Wnt signalling pathway, and hypoxia-inducible factor-1α (HIF-1α) [ 1 , 3 – 5 ]. In addition, the incidence of CVDs is significantly higher in cancer patients, and cancer survivors undergo a higher risk to develop CVDs [ 6 ], such as chronic heart failure [ 7 ]. Therefore, new diagnoses of malignancy in subjects with pre-existing HF can often occur, requiring a complex and early integrated cardio-oncological approach for their clinical management.…”