Role of P53 Gene in Oncogenesis from Chronic Lymphocytic Leukemia

摘要

Objective of this study is to present the latest researches in the field of molecular medicine, in terms of Chronic Lymphocytic Leukemia (CLL), emerged from the P53 gene deletion in human lymphoma genome. Method In recent years proved that the best technique in the investigation of malignant lymphocytes is the Fluorescence in situ hybridization (FISH). This method is used as an alternative to chromosomal banding, a conventional application in molecular medicine. Previous Results: In the literature it was registered, in previous years, on an international study, conducted on 109 cases of CLL, 79 cases (72.5%) who had more genetic abnormalities; the remaining 30 cases (27.5%) had normal results, using the technique Florescence in situ Hybridization, (FISH). The majority of patients, 67% (53.79) had a single anomaly and the remaining 33% had two or three genetic abnormalities. The band 14q32 /17p translocations in LLC genome, which appeared similar to some common, had demonstrated abnormalities involving IGH gene, located on chromosome14q32. Discussions: Identification of P53 gene mutations in regions of 17 chromosome of hematological neoplasm is important because these mutations have an impact on the clinical course of patients and requires an attitude adjustment therapeutic adequate. Restoring function to p53 can induce lymphoma, apoptosis. Recent, endogenous somatic gene therapy research is a basic of trial clinical and therapeutic trial. The DNA, is used to treat a disease arising as a result of mutations in chromosomal regions. In the past few years, this method has been included in the treatment of CLL, acute lymphocytic leukemia, [ALL], or multiple myeloma [MM]. Conclusion: The frequencies of P53 gene mutations and deletion in CLL can be categorized as individual biomarkers in proteomic and genomic profile for this type of leukemia that can be implemented in targeted patient treatment of personalized medicine.