**1. Introduction**

Myelodysplastic syndromes (MDSs) comprises a heterogeneous group of myeloid neoplasms, they are characterized by pancytopenia, bone marrow (BM) hyperplasia, dysplasia, and cytopenias of the peripheral blood. The blast count may be normal or elevated but is less than 20% in the bone marrow and peripheral blood. MDS are characterized by elevated risk of progression to secondary acute myeloid leukemia (AML) [1, 2].

MDS is caused by accumulation of genetic or epigenetic (such as promoter hypermethyltion) lesions, first it s occurred in an immature progenitor and provides proliferative advantage of the MDS clone over normal immature progenitors.

MDS progenitors leads abnormal terminal differentiation and capacity to resist to apoptosis. These two features explain the clinical consequences of blast accumulation and peripheral cytopenias. Microenvironmental changes and immune deregulation participate to this differentiation defect [3].

The purpose of this review is to overview the recent advances in the cytogenetics and genetics of MDS and related disorders.
