Introduction
Genetic alterations of acute lymphoblastic leukemia (ALL) involved in various signaling pathways are associated with the disease pathogenesis.Moreover,they may play a role as predictive biomarkers for selecting the treatment protocol and adjusting risk stratification.Inactivation of the tumor suppressor gene CDKN2Ain the 9p21.3 locus,which has been implicated in many cancer,can occurby deletion,methylation, or mutation[2].CDKN2A gene deletion is commonly present in pediatric ALL which can be detected by fluorescent in-situ hybridization(FISH)[3].It showed that CDKN2A deletion occurred in 21% BCP-ALL and 50% T-ALL patients[4].Under normal conditions,the CDKN2A gene encodes two proteins,p16INK4a and p14ARF.These two proteins specifically inactivate cyclin/CDK4/6 complexes that block cell division during the G1/S phase of the cell cycle[5].A lot of research found that the deletion of CDNK2A is not only associated with T-lineage ALL but also B-lineage ALL[4,6-7].
Despite the high frequency of CDKN2A deletion in pediatric ALL,the prognosis importance in pediatric ALL is still inconclusive.Most of the results thought the deletion of CDKN2A was associated with pediatric ALL recurrence[8-9].While Mirebeau D reported that inactivation of CDKN2A gene did not influence B-lineage acute lymphoblastic leukemia of childhood’ outcome in 2006[6].
In this article we tried to describe the clinical-biological characteristics and prognostic factors in pediatric ALL patients with CDKN2A deletion.
Methods