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Tumors and heart disease are two of the leading causes of human death. With the development of anti-cancer therapy, the survival rate of cancer patients has been significantly improved. But at the same time, the incidence of cardiovascular adverse events caused by cancer treatment has also been considerably increased, such as arrhythmia, left ventricular (LV) systolic and diastolic dysfunction, and even heart failure (HF), etc., which seriously affects the quality of life of cancer patients. More importantly, the occurrence of adverse events may lead to the adjustment or the cessation of anti-cancer treatment, which affects the survival rate of patients. Understanding the mechanism of cardiotoxicity (CTX) induced by antineoplastic drugs is the basis of adequate protection of the heart without impairing the efficacy of antineoplastic therapy. Based on current research, a large amount of evidence has shown that oxidative stress (OS) plays an essential role in CTX induced by antineoplastic drugs and participates in its toxic reaction directly and indirectly. Here, we will review the mechanism of action of OS in cardiac toxicity of antineoplastic drugs, to provide new ideas for researchers, and provide further guidance for clinical prevention and treatment of cardiac toxicity of anti-tumor drugs in the future., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Hydrogen (H2) has advantages that lead it to be used as a novel antioxidant in preventive and therapeutic applications. H2 can permeate into biomembranes, cytosol, mitochondria and nuclei, and can be dissolved in water or saline to produce H2 water or H2‑rich saline. H2 selectively reduces oxidants of the detrimental reactive oxygen species (ROS), including hydroxyl radicals (·OH) and peroxynitrite (ONOO‑), which serve a causative role in the promotion of tumor cell proliferation, invasion and metastasis, but do not disturb metabolic oxidation‑reduction reactions in cell signaling. Compared with traditional antioxidants, H2 is a small molecule that can easily dissipate throughout the body and cells; thus, it may be a safe and effective antioxidant for inflammatory diseases and cancer, since ROS usually initiates tumor progression. Treatment with H2 may involve correction of the oxidative/anti‑oxidative imbalance and suppression of inflammatory mediators. Therefore the present review will discuss the anti‑inflammatory and anti‑tumorigenic action of H2 via ROS. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Comment on Metformin sensitizes endometrial cancer cells to chemotherapy by repressing glyoxalase I expression" in the February 2013 issue.

Abstract: Obesity is generally acknowledged as a risk factor for endometrial cancer, as accumulated adipocytes partly contribute to the increased production of estrogen which is involved in dysregulated cell growth and metastasis in early endometrial carcinogenesis. Thus we evaluated in this study expression of the fat mass and obesity-associated (FTO) gene in endometrial tumor tissues and further explored its role in β-estradiol (E2)-induced endometrial cancer cell proliferation and invasion. IHC staining showed that FTO overexpressed in endometrial carcinoma. Additionally, E2-induced FTO via activation of the PI3K/AKT and MPAK signal pathways contributed to enhanced proliferation and invasion. Therefore, this study provides a new insight on the mechanisms of E2-induced proliferation and invasion and the link between obesity and endometrial cancer, implying the possibility of using FTO as a potential therapeutic target for the treatment of endometrial cancer. [Copyright &y& Elsevier]