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Critical evaluation of how and when to include anthracyclines in preoperative chemotherapy is becoming more relevant in an era when the molecular genetic approach not only allows for the development of biologically targeted therapeutics, but also implies the ability to select the patients likely to benefit from certain cytotoxic agents. Changes in the copy number aberration (CNA) landscape of luminal B HER2- negative (HER2-) breast cancer (BC) during anthracycline-based neoadjuvant chemotherapy (NAC) regimens were studied in order to identify groups of potential CNA markers of objective response and CNA markers for predicting the development of hematogenous metastasis. Comparison of CNA frequencies depending on the response to NAC showed that objective response was observed in a larger number of deletions in the 11q22.3 and 11q23.1 loci ( p = 0.004). Comparison of CNA frequencies in groups of patients after treatment showed that hematogenous metastasis was observed with a greater number of amplifications in the 9p22.2 locus ( p = 0.003) and with a greater number of deletions in the 9p21.3 locus ( p = 0.03). Potential predictive CNA markers of objective response and prognostic CNA markers of hematogenous metastasis in anthracycline- based NAC regimens have been identified., (Copyright ® 2023 National Research University Higher School of Economics.)

Our genome consists not only of protein-coding DNA, but also of the non-coding part that plays a very important role in the regulation of all cellular processes. A part of the non-coding genome comes with non-coding RNAs (ncRNAs), and disruption of the functional activity of these RNAs may be associated with oncogenesis in various cancer types. There exist two types of ncRNAs: small and long non-coding RNAs, which are classified according to their transcript length. Long non-coding metastasis-associated lung adenocarcinoma transcript 1, MALAT1 RNA ( NEAT2 ), is a long non-coding RNA of particular interest. The aforementioned transcript takes part in the regulation of numerous cellular processes and pathogenesis of different malignant tumors, including breast tumors. This review focuses on experimental and clinical studies into the role of MALAT1 in carcinogenesis and the progression of breast cancer., (Copyright ® 2023 National Research University Higher School of Economics.)

Many factors are involved in carcinogenesis of the ovary, such human genetic and physiological characteristics as lifestyle, existing diseases of the reproductive system, and, as suggested, the human papillomavirus (HPV). It is well known that the human papillomavirus virus of high carcinogenic risk (HCR) plays a crucial role in the onset and development of cervical cancer, as well as cases of HPV positive breast cancer and endometrial cancer. The data on the presence of HPV in ovarian cancer are ambiguous: the researchers claim that there is no complete effect of the virus on the development of this type of cancer, and the detection of HPV in 60-80% of tumors. In this regard, there is a need to systematize the currently available research results on this controversial issue and conduct a meta-analysis of the association of HPV infection with the risk of ovarian cancer., (Copyright © 2021 Elsevier B.V. All rights reserved.)

The NF-kB1 gene belongs to the family of transcription factors that are involved in the regulation of a wide range of biological reactions. It has been established that NF-kB1 plays an important role in the regulation of immune responses, but more and more studies indicate that this gene is involved in the processes of oncogenesis and DNA repair. The product of this gene regulates the expression of genes involved in the development and progression of cancer. In recent years, numerous studies have been aimed at elucidating the functional consequences of the activation of NF-kB1, as well as its signaling mechanisms. In this regard, NF-kB1 is an interesting therapeutic target for a possible personalized approach in the treatment of cancer. This article provides an overview of modern clinical studies of the NF-kB1 gene, which acts as a predictive and prognostic marker in the treatment of cancer.

In 5 patients, a change in the genetic landscape from HPV16 positive high-grade squamous intraepithelial lesion (HSIL) to squamous cervical cancer was traced, which occurred in these patients within the period from 7 months to 5 years after diagnosing HSIL., Materials and Methods: The DNA from paraffin blocks of dysplasia tissue and the tumor that emerged afterwards was used for the study, which was analyzed using the OncoScan FFPE microarray Assay Kit Affymetrix (USA) for genome-wide determination of gene abundance and 65 key somatic driver mutations of oncogenes and tumor suppressor genes., Results: In the study of HSIL material, somatic mutations were observed in 4/5 cases, 18 different somatic driver mutations of the NRAS, EGFR, BRAF, KRAS, IDH2 oncogenes and TP53 suppressor genes were found and almost no CNA-Copy Number Aberration was identified. HSIL malignization is associated with the appearance of secondary driver mutations in oncogenes and tumor suppressor genes and a large number of structural and numerical CNA, the frequency of which correlates with the time of dysplasia malignization into cancer with a very high correlation coefficient r = 0.98, P = 0.004. The trees of dysplasia evolution into tumor were constructed for each patient., Conclusion: According to the results of the work, it is assumed that the initiation of the development of mucosa dysplastic changes is due to primary driver mutations. The formation of secondary driver mutations and CNA are genetic mechanisms of malignant transformation, while the scenarios of the evolution of dysplasia into a tumor are individual and very diverse., (Copyright © 2020. Published by Elsevier Inc.)

The review is devoted to assessing the prevalence of human papillomavirus (HPV) in combination with other viral agents for head and neck tumors (HNT). HPV is recognized as an etiological factor in the development of cervical cancer, but there is evidence that it may be involved in carcinogenesis in other locations, in particular the upper respiratory tract. However, HPV is not the most important factor in tumor growth and progression. Recently, many researchers have reported the presence of concomitant co-infection, affecting tumor progression. Of all the studies analyzed, only 3 studies showed the absence or low rates of co-infection in HNT: from the Czech Republic (0%), China (0.6%) and Japan (3%). Most often, HPV infection was detected together with the Epstein-Barr virus (EBV) - from 12.5 to 34.1% of cases. In Russia, the prevailing combination of viral co-infection was a combination of EBV and cytomegalovirus (9.5%) and a combination of EBV and herpes simplex virus (6.7%). Thus, the degree of incidence of HPV in HNT varies greatly, and the mechanisms of coinfection are poorly understood, which raises the question of whether HPV and concomitant infection can be involved in tumor progression. This makes further research in this direction relevant and promising.