title: Leptin promoter G-2548A genotypes and associated serum leptin levels in childhood acute leukemia at diagnosis and under high-dose steroid therapy.
abstract: Genotype/allele distributions of leptin promoter G-2548A polymorphism, serum leptin and insulin levels and body weight were not significantly different between 72 children (39 male/33 female; age range 1.08-16, median 6 years) with acute leukemia (56 acute lymphoblastic leukemia [ALL]/16 acute non-lymphoblastic leukemia [ANLL]) at diagnosis and 70 age- and sex-matched controls (p > 0.05). The - 2548GG genotype was associated with the highest leptin levels in controls and patients with acute leukemia after 7-day high-dose methylprednisolone (HDMP) therapy (p < 0.05), while no significant association of genotype with leptin levels was detected in patients at diagnosis (p > 0.05). One-week HDMP therapy in patients carrying the - 2548G allele caused a significant increase in leptin levels and body weight (p < 0.001), whereas increases in those carrying the - 2548AA genotype were insignificant (p > 0.05). Decreases in white blood cell counts of patients after therapy were insignificant in - 2548GG (p > 0.05) yet significant in - 2548GA and - 2548AA (p < 0.05) genotypes. These results revealed no association of leptin genotype with the etiology of childhood acute leukemia but a possible association with leptin levels and effects of HDMP therapy.
authors.affiliation: Division of Hematology, Department of Pediatrics, Faculty of Medicine, Hacettepe University, Sihhiye, Ankara, Turkey.
authors.forename: Betul
authors.initials: B
authors.lastname: Tavil
authors.forename: Gunay
authors.initials: G
authors.lastname: Balta
authors.forename: Eser Lay
authors.initials: EL
authors.lastname: Ergun
authors.forename: Serdar
authors.initials: S
authors.lastname: Ozkasap
authors.forename: Murat
authors.initials: M
authors.lastname: Tuncer
authors.forename: Bahattin
authors.initials: B
authors.lastname: Tunc
authors.forename: Mualla
authors.initials: M
authors.lastname: Cetin
authors.forename: Aytemiz
authors.initials: A
authors.lastname: Gurgey
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D003967:Diarrhea / Q000139:chemically induced; D004305:Dose-Response Relationship, Drug; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D005938:Glucocorticoids / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans; D006943:Hyperglycemia / Q000139:chemically induced; D007223:Infant; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood / Q000235:genetics*; D007938:Leukemia / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy* / Q000235:genetics*; D008297:Male; D008775:Methylprednisolone / Q000009:adverse effects / Q000627:therapeutic use*; D020641:Polymorphism, Single Nucleotide; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000097:blood / Q000188:drug therapy / Q000235:genetics; D011401:Promoter Regions, Genetic / Q000235:genetics*; D011446:Prospective Studies; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D005938:Glucocorticoids; D007328:Insulin; D020738:Leptin; D008775:Methylprednisolone