Sulfotransferase 1A1 Arg(213)His polymorphism and prostate cancer risk

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ARSLAN S., SİLİĞ Y., PINARBAŞI H.

EXPERIMENTAL AND THERAPEUTIC MEDICINE, cilt.2, sa.6, ss.1159-1162, 2011 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 2 Sayı: 6
  • Basım Tarihi: 2011
  • Doi Numarası: 10.3892/etm.2011.334
  • Dergi Adı: EXPERIMENTAL AND THERAPEUTIC MEDICINE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.1159-1162
  • Anahtar Kelimeler: sulfotransferase 1A1, prostate cancer, genetic polymorphism, Turkish population, CYTOSOLIC SULFOTRANSFERASES, PHENOL SULFOTRANSFERASES, GENETIC POLYMORPHISMS, SULT1A1 POLYMORPHISM, BREAST-CANCER, ASSOCIATION, ACTIVATION, GENOTYPE, POPULATION, SULFATION
  • Sivas Cumhuriyet Üniversitesi Adresli: Evet

Özet

Sulfotransferase 1A1 (SULT1A1) is a member of the sulfotransferase family that plays an important role in the biotransformation of numerous carcinogenic and mutagenic compounds through sulfation. A transition, G to A at position 638, in the SULT1A1 gene, results in the Arg(213)His change. This single nucleotide polymorphism reduces the activity and thermostability of the SULT1A1 enzyme. In the present study, the relationship between the SULT1A1 Arg(213)His polymorphism and prostate cancer was investigated using PCR-RFLP. No significant difference in genotype and allele distribution was noted between the prostate cancer and control populations (P=0.072; P=0.099, respectively). The risk of prostate cancer in individuals carrying the SULT1A1*2 allele (His(213) allele) was determined by combining the SULT1A1*1/SULT1A1*2 (Arg/His(213)) and SULT1A1*2/SULT1A1*2 (His/His(213)) genotypes. No association was observed between SULT1A1 Arg(213)His polymorphism and prostate cancer incidence (P=0.24; OR, 1.36; 95% CI, 0.84-2.25). However, the His(213) allele was found to increase the risk of prostate cancer by 1.36-fold. In smoker and non-smoker populations, no significant relationship was determined between the prostate cancer and control population (P=0.45; P=0.34, respectively).