PMID- 17717965
OWN - NLM
STAT- MEDLINE
DCOM- 20070919
LR  - 20181201
IS  - 1176-9114 (Print)
IS  - 1178-2013 (Electronic)
IS  - 1176-9114 (Linking)
VI  - 1
IP  - 3
DP  - 2006
TI  - Asparaginase (native ASNase or pegylated ASNase) in the treatment of acute 
      lymphoblastic leukemia.
PG  - 241-54
AB  - The discovery of the tumor-inhibitory properties of asparaginase (ASNase) began 
      in the early 1950s with the observation that guinea pig serum-treated 
      lymphoma-bearing mice underwent rapid and often complete regression. About 4000 
      cases of acute lymphoblastic leukemia (ALL) are diagnosed very year in the US and 
      many more through out the world. The majority of these cases are in children and 
      young adults, making ALL the most common form of malignancy in these age groups. 
      The treatment protocols of ALL are complex and use 6-12 drugs. Consequently, the 
      improvement in the protocol design has improved significantly the success rate 
      for long-term event-free survival in the past 20-30 years, which is now 
      approximately 75% for patients afflicted with the higher risk ALL features and 
      just above this percentage for patients with standard or good features. Despite 
      this success, approximately 15% of patients die from ALL, making leukemic relapse 
      the most common cause of treatment failure in pediatric oncology. ASNases have 
      been the cornerstone of ALL therapies since the late 1970s. Native or pegylated 
      L-asparaginase (ASNase or PEG-ASNase) are highly specific for the deamination of 
      L-asparagine (Asn) to aspartic acid and ammonia. Depletion of Asn leads to a 
      nutritional deprivation and inhibition of protein biosynthesis, resulting in 
      apoptosis in T-lymphoblastic leukemias, which require Asn from external sources. 
      The reactions of the host exposed to repeated ASNase treatments as well as the 
      up-regulation of the mammalian enzymes to overcome the ASN-depletion toxic 
      condition are of significant importance and may make us relearn the lessons on 
      this important antileukemic drug.
FAU - Avramis, Vassilios I
AU  - Avramis VI
AD  - CHLA, Department of Pediatrics, Division of Hematology/Oncology, Keck School of 
      Medicine, Childrens Hospital Los Angeles, Los Angeles, CA 90027, USA. 
      vavramis@chla.usc.edu
FAU - Tiwari, Prakash Nidhi
AU  - Tiwari PN
LA  - eng
PT  - Journal Article
PT  - Review
PL  - New Zealand
TA  - Int J Nanomedicine
JT  - International journal of nanomedicine
JID - 101263847
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Drug Carriers)
RN  - 3WJQ0SDW1A (Polyethylene Glycols)
RN  - EC 3.5.1.1 (Asparaginase)
SB  - IM
MH  - Antineoplastic Agents/administration & dosage/chemistry/pharmacokinetics
MH  - Asparaginase/*administration & dosage/chemistry/*pharmacokinetics
MH  - Drug Carriers/*chemistry
MH  - Humans
MH  - Polyethylene Glycols/*chemistry
MH  - Precursor Cell Lymphoblastic Leukemia-Lymphoma/*drug therapy/*metabolism
PMC - PMC2426805
EDAT- 2007/08/28 09:00
MHDA- 2007/09/20 09:00
PMCR- 2007/01/01
CRDT- 2007/08/28 09:00
PHST- 2007/08/28 09:00 [pubmed]
PHST- 2007/09/20 09:00 [medline]
PHST- 2007/08/28 09:00 [entrez]
PHST- 2007/01/01 00:00 [pmc-release]
PST - ppublish
SO  - Int J Nanomedicine. 2006;1(3):241-54.