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| Content Provider | PubMed Central |
|---|---|
| Author | Deepika, Bhatla Gerbing, Robert B. Alonzo, Todd A. Conner, Heather Ross, Julie A. Meshinchi, Soheil Zhai, Xiaowen Zamzow, Tiffany Mehta, Parinda A. Geiger, Hartmut John, Perentesis Davies, Stella M. |
| Abstract | Cytosine arabinoside (ara-C) is irreversibly deaminated by cytidine deaminase (CDD) to a nontoxic metabolite. A common polymorphism, A79C, in CDD changes a lysine residue to glutamine resulting in decreased enzyme activity. We determined CDD A79C genotypes for 457 children with AML treated on CCG 2941 and 2961 and analyzed the impact of CDD genotype on therapy outcomes. Post-Induction treatment related mortality (TRM) was significantly elevated in children with the CC genotype (5 year TRM 17 ± 13% CC vs 7 ± 4% AA, 5 ± 4% AC, p= 0.05). This was more notable in children who received IDA-FLAG (ara-C= 7590 mg/m2) (5 year TRM 24 ± 21% CC vs 6 ± 6% AA, 6 ± 7% AC, p=0.07) as consolidation therapy compared to IDA-DCTER (ara-C= 800 mg/m2) (5 year TRM 15 ± 20% CC vs 8 ± 6% AA, 4 ± 6% AC; p=0.29). Relapse-free survival was non-significantly increased in children with the CC genotype treated with IDA-FLAG (76 ± 20% CC vs 59 ± 12% AA and 55 ± 14% AC; p= 0.40). These data indicate that children with a low activity CDD genotype are at increased risk of treatment-related mortality with Ara-C based therapy for AML. |
| Related Links | http://dx.doi.org/10.1111/j.1365-2141.2008.07461.x |
| Starting Page | 388 |
| File Format | |
| ISSN | 13652141 |
| e-ISSN | 13652141 |
| Journal | British journal of haematology |
| Issue Number | 3 |
| Volume Number | 144 |
| Language | English |
| Publisher Date | 2009-02-01 |
| Access Restriction | Open |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Hematology |
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