The role of cytogenetic and molecular genetic alterations of TP53 in the oncogenesis of clonal diseases of the hematopoietic and lymphatic systems literature review

The integration of new treatment methods of the hematopoietic and lymphatic system neoplasms has led to a significant improvement in patient survival rates. However, a significant part of patients has a genetic change which sharply reduce the effectiveness of therapy and survival. One of these changes is a genetically determined dysfunction of the p53 transcription factor. The purpose of this review is to analyze the data of modern literature on the role of molecular changes in the TP53 gene and chromosomal aberrations of the 17p13.1 locus in the occurrence and progression of malignant neoplasms of the hematopoietic and lymphatic system. The review is based on an analysis of publications indexed in PubMed, Medline, and other databases. Literature data indicate the pathogenetic significance of TP53 genetic alterations in all phases of hemoblastosis oncogenesis. The absence of normal p53 determines cell malignancy and malignant progression of hemoblastosis and gives tumor cells an "evolutionary advantage" manifested by faster growth, accumulation of new mutations, and resistance to chemotherapeutic agents. The presence of a TP53 deletion or molecular mutation indicates an extremely unfavorable course of hemoblastosis, requiring special treatment strategies and careful monitoring. Thus, genetic changes in TP53 are the most important marker that allows predicting the risk group, response to treatment and survival of patients with various malignant neoplasms of the hematopoietic and lymphatic system, therefore, its detection should be a mandatory item in the algorithm of diagnostic and monitoring studies of hematological patients.