Abstract. Oncocytic follicular adenomas (FAs) of the thyroid are neoplasms of follicular cell origin that are predominantly composed of large polygonal cells with eosinophilic and granular cytoplasm. However, the pathological characteristics of these tumors are largely unexplored. Both the initiation and progression of cancer can be caused by an accumulation of genetic mutations that can induce genomic instability. Thus, the aim of this study was to evaluate the extent of genomic instability in oncocytic FA. As the presence of p53-binding protein 1 (53BP1) in nuclear foci has been found to reflect DNA double-strand breaks that are triggered by various stresses, the immunofluorescence expression pattern of 53BP-1 was assessed in oncocytic and conventional FA. The association with the degree of DNA copy number aberration (CNA) was also evaluated using array-based comparative genomic hybridization. Data from this study demonstrated increased 53BP1 expression (i.e., "unstable" expression) in nuclear foci of oncocytic FA and a higher incidence of CNAs compared with conventional FA. There was also a particular focus on the amplification of chromosome 1p36 in oncocytic FA, which includes the locus for Tumor protein 73, a member of the p53 family implicated as a factor in the development of malignancies. Further evaluations revealed that unstable 53BP1 expression had a significant positive correlation with the levels of expression of Tumor protein 73. These data suggest a higher level of genomic instability in oncocytic FA compared with conventional FA, and a possible relationship between oncocytic FA and abnormal amplification of Tumor protein 73.Key words: Thyroid oncocytic tumor, 53BP1, DNA damage response, Genomic instability plasms of follicular cell origin predominantly, or entirely, composed of large polygonal cells with oxyphilic features related to the presence of eosinophilic and granular cytoplasm that is rich in mitochondria [1][2][3]. Encapsulated thyroid lesions with no evidence of capsular or vascular invasion and no nuclear features of papillary carcinoma are diagnosed as onco-

We studied the intensity of free radical processes in organs (liver, spleen, thymus, lymph nodes of the small intestine, and adrenal glands) and cells (lymphocytes) in the delayed period after combined exposure to a sublethal dose of γ-radiation (6 Gy) and asbestos dust particles. Combined exposure was followed by accumulation of LPO metabolites (diene conjugates and malonic dialdehyde) in homogenates of the studied organs and resulted in antioxidant defense failure in experimental animals. Ionizing radiation have a pivotal role in these processes.

Aim.To determine the severity of chronic kidney disease (CKD) in patients after acute coronary syndrome (ACS).Material and methods.The study was conducted in Semey (Semipalatinsk), East Kazakhstan region. The case histories of patients with ACS who were admitted to the University Hospital of the State Medical University (Semey State Medical University) of the East Kazakhstan Region for 1 year were studied. A total of 659 case histories were analyzed, of which 263 were patients with myocardial infarction (MI), and 396 were patients with unstable angina (UA). The diagnostic criteria for CKD were: proteinuria, levels of creatinine, glomerular filtration rate (GFR) <60 ml/min/1,73 m2. CKD stage was determined by the parameters of GFR.Results.The average proteinuria in patients with MI (Me=0,033) were higher than in patients with UA (Me=0,00), U=39564,5, Z=-5,579 p=0,000. The average values of creatinine in patients with MI were 10,26 mmol/l higher than in patients with UA (t=3,333, df=657, p=0,001). The mean GFR values in patients with MI were lower by 4,69 L/min/1,73 m2 than in patients with UA (t=-3,794, df=657, p=0,000. The highest percentage of CKD in patients with ACS were in stage 2-3, the second stage of CKD was more often diagnosed in patients with UA.Conclusion.The results of study allowed us to characterize the severity of CKD in patients undergoing ACS. We consider that widespread introduction of international and national clinical guidelines on the diagnosis, treatment and prevention of CKD in patients undergoing ACS is needed.