Blood: Relationship between ASNS methylation abnormality and sensitivity of celidate amidamide enzyme therapy in children with BCP-ALL

Chromosome nuclear type: Refers to all chromosomes in an individual cell, arranged by its size, morphological characteristics in order of the composition of the image called chromosome nucleotypeUnder normal circumstances, the nucleotype of a single cell can generally represent the nuclear type of that individualnucleotype is an important prognosis factor for acute lymphoblastic leukemia (BCP-ALL) in children, but the mechanism of pharmacogenomics is not clearTenomidethase is an integral part of the BCP-ALL chemotherapy regimen in childrenWinteramide therapy can deplete serum-day winteramidenormal hematopoietic cells can produce midiamide through the activity of the Asnline synth (ASNS), but ALL cells are unable to synthesize a sufficient amount of tianchomideThe ASNS gene has a classic CpG island, located in its promoterTherefore, ASNG's CpG island methylation may be an epigenetic mechanism of ASNS gene silencing in BCP-ALLin order to gain insight into the drug genomics of thetherapies of tiandonamide enzyme therapy, Watanabe et alstudied the relationship between ASNS methylation and the sensitivity of the tinmide enzymeASNS CpG island is mostly unmethylated in normal hematopoietic cells, but its allele-specific methylation occurs in BCP-ALL cellsThe ASNS gene is located on 7q21, an evolutionaryly conservative cluster of imprinted geneschildren's ASNS methylation in BCP-ALL was associated with abnormal methylation of the imprinted gene cluster on 7q21Abnormal methylation of asnas and homogenous imprinted gene clusters in mice from ETV6-RUNX1 was also confirmedin the three children's BCP-ALL queues, ASNS is highly methylated in BCP-ALL with a good nuclear type, while most of the BCP-ALL with poor prognostic nuclear type is not methylatedASNS high methylation, by reducing asNS gene and protein expression levels, is associated with high l-tthanamide sensitivity in BCP-ALL, the results of this study show that ASNS gene silencing due to imprinting gene abnormalities is the drug genetic mechanism of the specific activity of leukemia in BCP-ALL in the therapy of the tummy amidamide enzyme therapy