Abstract
Aim of this study is to present the latest researches in the field of molecular medicine, in terms of treatments in malignant hemopathies, emerged from the P53 gene deletion in human lymphoma genome. Method: In recent years proved that the best techniques in the investigation of malignant lymphocytes are the Flow Cytometry, Elisa, ICT and Fluorescence in Situ Hybridization (FISH). This method is used as an alternative to chromosomal banding, a conventional application in molecular medicine. Discussion: 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.
Highlights
B-cell chronic lymphocytic leukemia (B-CLL) is one of the most common hematologic malignant diseases which had especially to the elderly
The flux of glucose is directed in a path lipogenic de novo, which is regulated in part by the enzyme phosphoinositol-3 kinase (PI-3K) activation dependent on the ATP-citrate lyase (ACL), which is a cytosolic enzyme which catalyzes the production of acetyl CoA citrate
Aim The objective of this study is to present the latest researches in the field of molecular medicine, in terms of CLL, emerged from the P53 gene with deletions or translocations in human lymphoma genome and the prognostic and treatment of this diseases, in function of damages of P53 gene
Summary
B-cell chronic lymphocytic leukemia (B-CLL) is one of the most common hematologic malignant diseases which had especially to the elderly. The flux of glucose is directed in a path lipogenic de novo, which is regulated in part by the enzyme phosphoinositol-3 kinase (PI-3K) activation dependent on the ATP-citrate lyase (ACL), which is a cytosolic enzyme which catalyzes the production of acetyl CoA citrate. Phosphatase-tensin homolog (PTEN) is a tumor suppressor protein that regulates enzyme phosphoinositol-3 kinase (PI3K). Several mutations or loss of function of PTEN affects lipid phosphatase activity which leads to development of a variety of cancers. Of the three residues of component PTEN, residue R-335 was observed as important to interact with the membrane cellular, in common with several other mutations in the germ line and was associated with cancers inherited [Figure 1], [2]
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