We investigated whether an altered individual glucocorticoid sensitivity due to particular glucocorticoid receptor single-nucleotide polymorphisms (SNPs) (N363S, ER22/23EK, and Bcl-1) influences the susceptibility to steroid-related toxicities, prognostic factors, and survival rates in children with acute lymphoblastic leukemia.
Homozygosity for CCND1 A allele was associated with ALL patients and was a risk factor for ALL development, while the presence of the A allele, whether in homozygous or heterozygous state was associated with breast cancer cases and was a risk for breast cancer .Homozygosity for CCND1 G allele was associated with the control group.
We have demonstrated that WNT5A, a putative tumour suppressor gene in ALL, is silenced by methylation in this disease and that this epigenetic event is associated with upregulation of CYCLIN D1 expression and confers poor prognosis in this group of patients.
This study shows that children with acute lymphoblastic leukaemia (ALL) who are homozygous for the CCND1 A variant have a lower probability of event-free survival (P = 0.006) compared to carriers of the G variant.
The expression of CD5 and cyclin D1 may need to be routinely determined on ALL cases with mature B-cell phenotype and non-L3 morphology to facilitate timely diagnosis of blastoid MCL and institution of suitable management.
Patients with ALL who were strongly positive for cyclin D1 had a lower probability of remaining in first continuous remission than ALL patients who were negative or weakly positive for this trait.