Antrasiklin Bazlı Kemoterapi Alan Meme Kanseri Hastalarında Kardiyotoksisite Belirteci Olarak Plazma Mikrorna34a Düzeylerinin Değerlendirilmesi

Abstract

Breast cancer is the most common cancer in women all over the world. Advances in early diagnosis and effective treatment have resulted in a significant prolongation of the life expectancy of patients with breast cancer. An increase in cardiovascular disease was detected in this population with an increase in breast cancer survivors. The high rate of cardiovascular morbidity and mortality in breast cancer survivors has increased the interest of oncologists to long-term side effects of chemotherapies. Anthracyclines, which are frequently used in many stages of breast cancer treatment, have well known side effects. Anthracycline-induced cardiotoxicity is often seen lately, 10 to 15 years after treatment. Although anthracyclines are well known for their cardiac damaging effects, there is no biomarker currently available to detect it early on. Some microRNAs have been found to be cardiotoxicity markers in animal studies. The purpose of this study is to assess whether plasma levels of microRNA34a(miR34a) can predict cardiotoxicity in breast cancer patients who will receive anthracycline-based chemotherapy. Forty-one breast cancer patients who will receive anthracycline-based chemotherapy for the first time are included in the study. Before and after taking chemotherapy, patients were examined for cardiac troponin-I, miR34a, and precursor miR34a levels, and echocardiographic strain analyzes were performed. There was a statistically significant increase in troponin-I, miR34a and pre-miR34a levels after treatment with anthracyclines. The mean increase in miR34a and pre-miR34a was 2.5 and 2.3 fold, respectively. Echocardiographic analysis of patients showed a significant decrease in global longitudinal strain (GLS) measurements compared to baseline after anthracycline treatment. An increase in the levels of miR34a / pre-miR34a was detected in patients who were estimated to have cardiac damage according to GLS replacement, but this increase was not statistically significant. The increased levels of miR34a / premiR34a levels, not miR34a, suggests a relationship between doxorubicin treatment and miR34a biogenesis. This is the first study in which miR34a and precursor pre-miR34a were evaluated together as anthracyclin-induced cardiotoxicity markers. Longer-term and larger-scale studies are needed to understand the role of miR34a in the development of cardiotoxicity and to be a biomarker.