Autophagy and epithelial-to-mesenchymal transition (EMT) are the main biological processes involved in tumor progression, and are closely linked. On the one hand, activation of autophagy provides energy and essential nutrients for EMT during the metastases spreading, which is required for tumor cells survival in adverse environmental conditions. On the other hand, autophagy, acting as a tumor suppressor, tends to inhibit metastasis by selectively suppressing the transcription factors of EMT in the early stages. Therefore, inhibition of EMT by inhibitors or inducers of autophagy may be a new strategy for antitumor therapy.
Thus, the aim of this review is to highlight current knowledge about the crosstalk between autophagy and EMT processes in tumor progression and to summarize data supporting the necessity of parallel regulation of two processes through signaling pathways.

In the treatment of breast cancer, the neoadjuvant chemotherapy is vitally important and the evaluation of its effectiveness is crucial for determining the further therapy treatment, as well as the prognosis of the disease. This review provides current data of the physical, instrumental, morphological, molecular biology and genetics analysis used for the estimation of the neoadjuvant treatment effectiveness. Thus, review discusses the data concerning association of the disease peculiarities with the efficient therapeutic response to neoadjuvant chemotherapy including characteristics of patients (age, status of regional lymph nodes, presence of the lymphovascular invasion) and tumors (size, histological type, degree of differentiation, severity of the lymphoid tumor infiltration, molecular biological and genetic peculiarities). Particular attention is paid to such a promising predictive marker of the breast cancer response to chemotherapy as the level of tissue hypoxia. This section discusses the currently known mechanisms that might enable the effect of tissue hypoxia on the sensitivity of the tumor to drug treatment. The prospects for the use of a comprehensive analysis of predictive markers of the effectiveness of chemotherapeutic treatment are discussed.

Background. One of the main reasons of the ineffectiveness of chemotherapy is still considered to be the formation of the multidrug resistance phenotype of the tumor due to the expression of energy-dependent proteins of ABC transporters. Our previous studies for some ABC genes have established that the expression of these genes correlates with the effectiveness of neoadjuvant chemotherapy (NAC). Some of the clinical studies indicate that ABC transporters can influence not only the formation of chemoresistance in the tumor, but also the progression, invasion and metastasis of the tumor node.
Objective: to evaluate the level of transcription of all 49 known ABC genes in a breast tumor before and after treatment and their prognostic significance.
Materials and methods. The study included 31 patients with a diagnosis of stage IIA – IIIB breast cancer. RNA was isolated from paired samples of tumor tissue before and after NAC. A microarray study of all tumor samples was performed on Clariom^ТМ S Assay, human microarrays. Using microarray studies, the expression of 49 genes of the ABC transporter family was studied. Analysis of the microchip data was carried out using the program Transcriptome Analysis Console (TAC) software 4.0.
Results. It was found that changes in the expression (increase/decrease during NAC) of the ABCA5, ABCA7, ABCB1, ABCB4, ABCB11, ABCC1, ABCC10, ABCC11, ABCG1, ABCG2, ABCG4, ABCG5, ABCG8 genes are statistically significantly associated with the response to NAC. In addition, the prognostic significance of ABCB1 and ABCB4 gene expression was established. Survival analysis showed that 5-year survival rates in patients with high gene expression of ABCB1 and ABCB4 are lower compared to patients with low expression of these genes (log-rank-test p = 0.001 and 0.04 respectively).
Conclusion. Data were obtained on the relationship of gene expression of the ABC transporter family with the effect of NAC in patients with breast cancer and the outcome of the disease. The prognostic potential of the ABCB1 and ABCB4 genes in patients with breast cancer has been established.

Background. The search for molecular markers of colon diseases allowing highly specific and sensitive identification and differentiation of pathological processes is a clinically important problem. Expression levels of genes responsible for proliferation can reflect the changes in the affected tissues.
The study objective is to perform comparative analysis of molecular and genetic markers of proliferative activity in benign and malignant neoplasms of the colon.
Materials and methods. Analysis of the changes in proliferation markers (CCND1, с-MYC, Ki-67, HER2neu, TERT) in adenocarcinoma of the colon (n = 259), resection margin (about 15–20 cm from the tumor lesion) (n = 251), unchanged colon mucosa from healthy donors (n = 247), polyps (n = 28), unchanged colon mucosa intestinal polyposis (10–15 cm from the polyp) (n = 75) was performed using RT-PCR.
Results and conclusion. It was shown that morphologically unchanged tissue of intestinal mucosa in malignant tumors has significant differences from normal tissue of healthy donors. Significant differences in the level of expression of genes responsible for the processes of proliferation, с-MYC, CCND1, TERT were found in benign hyperproliferative diseases (polyps). Moreover, these changes were specific to the type of pathological process, which allows us to consider these genes as the most promising candidates in the development of a differential method for diagnosing colon diseases.

Background. Currently, little is known about the specific microRNAs involved in the development of cervical intraepithelial neoplasia (CIN1, 2, 3) and the transition to cancer in situ (CIS). Our meta-analysis allowed us to isolate 8 microRNAs (hsa-miR-1246, hsa-miR- 145-5p, hsa-miR-196b-5p, hsa-miR-34a-5p, hsa-miR-20a-5p, hsa-miR-21-5p, hsa-miR-375-5p, hsa-miR-96-5p) with potential significance in the progression of precancerous diseases to cervical cancer.
Objective: to analyze the expression features of hsa-miR-1246, hsa-miR-145-5p, hsa-miR-196b-5p, hsa-miR-34a-5p, hsa-miR-20a-5p, hsa-miR-21-5p, hsa-miR-375-5p, hsa-miR-96-5p and their target genes, as well as genes associated with them in common signaling pathways in the tissues of the cervix in patients with CIN1–3 and CIS.
Materials and methods. To assess the expression level of microRNA and matrixRNA, the quantitative polymerase chain reaction in real time method was used. Data analysis was carried out in the Python programming language using the SciPy library. Search for target genes was performed using the TarPmiR algorithm and the overrepresentation of microRNAs in signaling pathways (Over-Representation Analysis) was analyzed. To identify genes associated with target genes in common signaling pathways, GIANT (Genome-scale Integrated Analysis of gene Networks in Tissues) and network integration with several associations algorithms were used.
Results. For microRNAs miR-145, miR-196b, miR-34a, miR-20a, miR-21, miR-375 and miR-96 a decrease in expression was found in the subgroup of patients with CIS, while for 4 microRNAs (miR-145, miR-34a, miR-20a and miR-375), an increase in the expression level was found for CIN1, 2. The detected features of microRNA expression in subgroups of patients with CIN1–3 and CIS also affected the expression of their target genes (CDKN2A, MKI67, TOP2A and CD82), as well as the genes associated with them in common signaling pathways (PGK1, THBS4 (TSP4) and ECM1).
Conclusion. Thus, the study revealed that each degree of CIN is characterized by its own specific molecular profile – the differential expression of microRNAs, their target genes and the genes associated with them in the general signaling pathways.