Please use this identifier to cite or link to this item:
10.7314/APJCP.2014.15.22.9707
Title: | Lack of association between polymorphisms in genes MTHFR and MDR1 with risk of childhood acute lymphoblastic leukemia |
Authors: | Kreile, Madara Rots, Dmitrijs Piekuse, Linda Cebura, Elizabete Grutupa, Marika Kovalova, Zhanna Lace, Baiba Rīga Stradiņš University |
Keywords: | Childhood cases;Lymphoblastic leukemia;MDR1;MTHFR;Polymorphisms;3.2 Clinical medicine;3.3 Health sciences;1.1. Scientific article indexed in Web of Science and/or Scopus database;Epidemiology;Oncology;Public Health, Environmental and Occupational Health;Cancer Research;SDG 3 - Good Health and Well-being |
Issue Date: | 2014 |
Citation: | Kreile , M , Rots , D , Piekuse , L , Cebura , E , Grutupa , M , Kovalova , Z & Lace , B 2014 , ' Lack of association between polymorphisms in genes MTHFR and MDR1 with risk of childhood acute lymphoblastic leukemia ' , Asian Pacific Journal of Cancer Prevention , vol. 15 , no. 22 , pp. 9707-9711 . https://doi.org/10.7314/APJCP.2014.15.22.9707 |
Abstract: | Background: Acute lymphoblastic leukemia (ALL) is a complex disease caused by interactions between hazardous exogenous or/and endogenous agents and many mild effect inherited susceptibility mutations. Some of them are known, but their functional roles still requireinvestigation. Age is a recognized risk factor; children with disease onset after the age of ten have worse prognosis, presumably also triggered by inherited factors. Materials and Methods: The MDR1 gene polymorphisms rs1045642, rs2032582 and MTHFR gene polymorphisms rs1801131 and rs1801133 were genotyped in 68 ALL patients in remission and 102 age and gender matched controls; parental DNA samples were also available for 42 probands. Results: No case control association was found between analyzed polymorphisms and a risk of childhood ALL development. Linkage disequilibrium was not observed in a family-based association study either. Only marginal association was observed between genetic marker rs2032582A and later disease onset (p=0.04). Conclusions: Our data suggest that late age of ALL onset could be triggered by mild effect common alleles. |
DOI: | 10.7314/APJCP.2014.15.22.9707 |
ISSN: | 1513-7368 |
Appears in Collections: | Research outputs from Pure / Zinātniskās darbības rezultāti no ZDIS Pure |
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