| Literature DB >> 26101161 |
Farzaneh Ghazavi1, Tim Lammens2, Nadine Van Roy3, Bruce Poppe3, Frank Speleman3, Yves Benoit2, Pieter Van Vlierberghe3, Barbara De Moerloose4.
Abstract
B-Cell precursor acute lymphoblastic leukemia (BCP-ALL) arises from recurrent genetic insults that block precursor B-cell differentiation and drive aberrant proliferation and cell survival. Risk-adapted intensive chemotherapy is effective in curing the majority of children with BCP-ALL (>85%), but some children, not considered "high risk" and treated accordingly, experience a hematologic relapse. Moreover, survival rates in adults are significantly lower (∼40%) than those in children. Recent developments in genomewide genetic analysis have provided a wide range of chromosomal and genomic abnormalities characterizing BCP-ALL, several of which are associated with patient outcome. These findings provide an opportunity to adapt risk stratification and treatment schedules and to identify new druggable targets. In this review, we discuss the established and novel genetic alterations in BCP-ALL, their molecular background, and their potential use in risk stratification and treatment of BCP-ALL.Entities:
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Year: 2015 PMID: 26101161 DOI: 10.1016/j.exphem.2015.05.015
Source DB: PubMed Journal: Exp Hematol ISSN: 0301-472X Impact factor: 3.084