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

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