Studying molecular mechanisms of carcinogenesis, including abnormalities of the homologous recombination (HR) system, is an important objective when studying malignization. Dysfunction of HR genes, such as BRCA1/2, contributes to genomic instability and the development of more aggressive tumor clones. The use of chemical carcinogens, such as dimethylbenz(a)anthracene (DMBA), allows one to simulate tumorigenesis processes and assess changes in expression of  repair genes. It is important to study such changes to understand the mechanisms underlying adaptation of tumor cells to genotoxic stress and develop personalized approaches to cancer treatment. The study aimed to assess the expression of major HR genes in chemotherapy-induced carcinogenesis in mice. The study involved female outbred ICR laboratory mice (CD-1; n = 20). Two groups of animals were formed: the control group and the treatment group that was administered DMBA. Histological analysis of autopsy specimens was conducted to identify tumors. Gene expression levels were assessed using RT-PCR, and testing for chromosomal aberrations was performed using digital PCR. Tumors were found in four animals. Zero expression of the genes Brca1, Brca2, Cdk12, Chek2, Palb2, Bard1, Brip1 and Rad paralogues was observed in three tumor samples. One sample showed high expression of the genes Cdk12 (14.3), Chek1 (27.6), Rad51d (38.5). Predominance of deletions in the test genes was reported in the majority of cases. Thus, tumorigenesis is associated with the decrease in expression of major repair genes, chromosomal aberration formation, which can contribute to the emergence of more aggressive clones and increase sensitivity to chemotherapy drugs.