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Tytuł:
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The impact of CYP2D6*4 and GSTP1 Ile105Val polymorphisms on the susceptibility to develop BCR-ABL1 negative myeloproliferative neoplasms.
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Autorzy:
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Daglar-Aday A; Division of Medical Genetics, Department of Internal Medicine, Istanbul Medical Faculty, Istanbul University, Capa, 34093, Istanbul, Turkey. .
Akadam-Teker B; Department of Medical Genetics, Faculty of Medicine, Giresun University, Giresun, Turkey.
Yonal-Hindilerden I; Division of Hematology, Department of Internal Medicine, Istanbul Medical Faculty, Istanbul University, Istanbul, Turkey.
Dermenci H; Division of Hematology, Department of Internal Medicine, Haydarpaşa Numune Training and Research Hospital, Istanbul, Turkey.
Sahin E; Department of Internal Medicine, Istanbul Medical Faculty, Istanbul University, Istanbul, Turkey.
Hindilerden F; Hematology Clinic, Istanbul Bakırkoy Sadi Konuk Training and Research Hospital, Istanbul, Turkey.
Yilmaz-Aydogan H; Department of Molecular Medicine, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey.
Ozturk O; Department of Molecular Medicine, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey.
Yavuz AS; Division of Hematology, Department of Internal Medicine, Istanbul Medical Faculty, Istanbul University, Istanbul, Turkey.
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Źródło:
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Molecular biology reports [Mol Biol Rep] 2020 Oct; Vol. 47 (10), pp. 7413-7420. Date of Electronic Publication: 2020 Sep 11.
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Typ publikacji:
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Clinical Trial; Journal Article
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Język:
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English
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Imprint Name(s):
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Original Publication: Dordrecht, Boston, Reidel.
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MeSH Terms:
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Mutation, Missense*
Polymorphism, Single Nucleotide*
Cytochrome P-450 CYP2D6/*genetics
Fusion Proteins, bcr-abl/*genetics
Glutathione S-Transferase pi/*genetics
Hematologic Neoplasms/*genetics
Myeloproliferative Disorders/*genetics
Adult ; Aged ; Alleles ; Amino Acid Substitution ; Female ; Follow-Up Studies ; Hematologic Neoplasms/epidemiology ; Humans ; Male ; Middle Aged ; Myeloproliferative Disorders/epidemiology ; Turkey/epidemiology
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Grant Information:
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23924 Bilimsel Araştirma Projeleri Birimi, Istanbul Üniversitesi
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Contributed Indexing:
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Keywords: CYP2D6*4; GSTP1 Ile105Val; Myeloproliferative neoplasms; Polymorphism; Xenobiotics
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Substance Nomenclature:
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0 (BCR-ABL1 fusion protein, human)
EC 1.14.14.1 (Cytochrome P-450 CYP2D6)
EC 2.5.1.18 (GSTP1 protein, human)
EC 2.5.1.18 (Glutathione S-Transferase pi)
EC 2.7.10.2 (Fusion Proteins, bcr-abl)
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Entry Date(s):
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Date Created: 20200912 Date Completed: 20210518 Latest Revision: 20210518
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Update Code:
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20240105
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DOI:
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10.1007/s11033-020-05796-7
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PMID:
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32918123
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Inter-individual variations in the genes encoding xenobiotic-metabolizing enzymes have been reported to alter susceptibility to various diseases involving hematological disorders. The purpose of this case-control study was to investigate the relationship between CYP2D6*4 and GSTP1 Ile105Val polymorphisms and the risk of developing BCR-ABL1 negative myeloproliferative neoplasms (MPN). PCR-RFLP was used for genotyping single nucleotide polymorphisms (SNP) in CYP2D6 and GSTP1 in 139 patients with MPN and 126 controls. There was a significantly increased risk for developing BCR-ABL1 negative MPN for the group bearing the CYP2D6*4 variant allele (X 2 : 4.487; OR 1.738; 95% CI 1.040-2.904; p = 0.034). The platelet count was higher in CYP2D6*4 allele carriers (p = 0.047). There was no association between the GSTP1 Ile105Val polymorphism and the risk of developing MPNs. MPN patients bearing the GSTP1 Ile105Val variant allele had a higher prevalence of bleeding complications (X 2 : 7.510; OR 4.635; 95% CI 1.466-14.650; p = 0.006). Our study provides new data that the CYP2D6*4 polymorphism may be associated with an increased risk to develop MPNs while the GSTP1 Ile105Val polymorphism does not show such an association. To our knowledge, the current study is the first to investigate the relationship between CYP2D6*4 and GSTP1 Ile105Val polymorphisms and the risk of developing MPNs in the Turkish population. Further studies with more patients and controls are needed to support our data.
