BACKGROUND: The potential relationship between pulmonary tuberculosis and lung cancer has been the subject of intense interest over the past few decades. Nevertheless, the features of the pathogenesis of concomitant pathology remain poorly studied. AIM: The ain of the study to develop an experimental model of the concomitant pathology of tuberculosis and lung cancer. MATERIALS AND METHODS: The study was performed on mice of the C57BL/6 line at the age of two months in four groups: 1st intact mice (n = 12), 2nd mice without a tumor infected with tuberculosis (n = 24), 3rd tumor-bearing mice not infected with tuberculosis (n = 23), 4th tumor-bearing mice infected with tuberculosis (n = 24). Individual and group parameters were evaluated using the SPSS Statistica v23 software package. RESULTS: Tumor was developed at the site of primary transplantation in all mice from groups 3 and 4, which was confirmed by visual assessment and the results of histological examination. Tumor growth in the main group was significantly less than in the control group of the tumor, which may be due to intoxication against the background of tuberculosis infection. All infected mice from groups 2 and 4 developed pulmonary tuberculosis, confirmed by computed tomography of the lungs, bacteriological and histological examination of lung samples. Mycobacterial load in the lungs was the highest in animals with concomitant pathology of tuberculosis and tumor. The survival rate of mice was determined to a large extent by tumor growth rather than by the progression of tuberculosis infection. CONCLUSIONS: The results of the study indicate the possibility of creating an experimental biological model of the concomitant pathology of tuberculosis and lung cancer in mice. The features of the course of the concomitant pathology were revealed: Lewis lung epidermoid carcinoma develops more slowly in tuberculosis infected animals than in the tumor control group; the development of the tuberculosis process in mice with a tumor occurs more intensively than in the tuberculosis infection control group. The survival rate of mice with concomitant pathology is determined more by the intensity of tumor growth than by the progression of tuberculosis.

Developing nanoformulations of antitumor drugs represents a critical priority in addressing key challenges of free drug administration such as low therapeutic efficacy, poor bioavailability, and severe side effects, including high systemic toxicity. In this study, mPEG-b-PCL block copolymers of different molecular weights were synthesized and applied to develop nanoformulations of the antitumor aziridine-functionalized 1,3,5-triazine derivative, dioxadet (DOD) via nanoprecipitation. The resulting DOD-loaded nanoparticles exhibited optimal characteristics for intravenous administration, and high encapsulation efficiency. The effect of mPEG-b-PCL molecular weight on drug encapsulation and release was investigated, and the results were elucidated through computational analysis of the molecular binding mechanism between DOD and PCL. Release profiles showed a sustained biphasic pattern. Determination of DOD concentration in blood of healthy rats indicated that the nanoformulation extended DOD’s circulation time. The empty nanoparticles were well-tolerated by both normal and cancer cells. The nanoformulation maintained inhibitory activity against A549 cells with an IC₅₀, comparable to that of free DOD. The antitumor efficacy and reduced toxicity of the optimized nanoformulation were demonstrated in mice using two ascitic tumor models (Ehrlich ascites carcinoma and L1210 lymphoid leukemia) and one solid tumor model (Lewis lung epidermoid carcinoma) with the greatest therapeutic effect observed against the solid tumor.