An Update - Chronic Myeloid Leukemia: An Interaction Between in Cells, Genes and Molecules View PDF

^*Faris Q Alenzi
Department Of Immunology, College Of Applied Medical Sciences, Prince Sattam Bin Abdulaziz University, Saudi Arabia

^*Corresponding Author:

Faris Q Alenzi
Department Of Immunology, College Of Applied Medical Sciences, Prince Sattam Bin Abdulaziz University, Saudi Arabia
Email:qalenzi@ksu.edu.sa

Published on: 2015-12-10

Abstract

In chronic myeloid leukemia (CML) proliferation is increased and resistance to apoptosis has been proposed as a mechanism accounting for myeloid cell expansion. Antiapoptotic effects, high levels of proliferation, insensitivity to negative regulators and defects in the adhesion mechanism between primitive progenitor cells and stromal cells are considered to result from expression of the p210BCR-AB fusion protein. These defects are therefore likely to be responsible for myeloid expansion. These mini-review update recent insights into cells, genes and molecules pathways employ to regulate immune responses as well as to correlate the presence and molecular profile of CML

Keywords

Leukemia; CD4+; CD25+; Exosomes

Introduction

Chronic myeloid leukemia (CML), effectively a cancer of white blood cells, involves an unregulated increase in the growth of myeloid cells in the bone marrow that leads to an accumulation of these cells in the blood. It represents 15-20% of all leukemia’s in humans. Even though the use of tyrokine kinase inhibitors, and multi-modal treatments, in CML have led to recent improvements in patient survival over the past decade, leukemic relapse remains a formidable clinical challenge meaning that that the quality of life of CML patients is often compromised, and that survival rates remain low, principally due to disease relapse