AI Article Synopsis
- Sinusoidal obstruction syndrome (SOS) is a potential complication for children receiving treatment for acute lymphoblastic leukemia (ALL) and may be influenced by certain genetic factors, particularly thiopurine methyltransferase (TPMT) activity and MTHFR genotype.
- Researchers studied specific genetic polymorphisms in TPMT and MTHFR among 351 patients in a clinical trial to understand their impact on SOS risk associated with thioguanine treatment.
- The findings indicated that variations in TPMT and MTHFR genotypes did not significantly change the risk of developing SOS in these patients.
Article Abstract
Sinusoidal obstruction syndrome is a complication of therapy for pediatric ALL and may be modified by thiopurine methyltransferase activity as well as by MTHFR genotype. We assessed TPMT *3A, *3B, *3C, and MTHFR C677T and A1298C germline genetic polymorphisms among 351 patients enrolled in the thioguanine treatment arm of CCG-1952 clinical trial. TPMT and MTHFR C677T genotypes were not associated with SOS risk. The combination of MTHFR and TPMT variant genotypes was not associated with SOS risk. These suggest that germline genetic variation in TPMT and MTHFR do not significantly alter SOS risk in patients exposed to thioguanine.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4283196 | PMC |
| http://dx.doi.org/10.1002/pbc.25057 | DOI Listing |
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