Summary
A homozygous gene deletion at the GST1 locus of genomic DNA isolated from peripheral blood was investigated for its relationship with several types of cancer using the polymerase chain reaction (PCR) technique. DNA samples were prepared from blood obtained from 128 healthy blood donors and 150 patients with cancer or chronic hepatitis. PCR primers were prepared based on the human cDNA sequence and the intron/exon sequences of the rat Yb2 gene. The amplified sequence between exons 5 and 6 including intron 5 showed very clearly the presence of absence of the GST1 gene, after electrophoresis in a 2% agarose gel. Segregation of the presence and absence of PCR product from samples of twins and their parents indicated that presence involves homozygous or heterozygous normal GST1 genotypes while absence invovles only homozygous gene deletion. The patients with stomach cancer had a significantly higher frequency of gene deletion than did the healthy controls (P< 0.005). Thus, GST1 deletion may be a possible genetic marker for early detection of a group at high risk of stomach cancer.
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References
Blin N, Stafford DW (1976) A general method for the isolation of high molecular weight DNA from eukaryotes. Nucleic Acids Res 3:2303–2308
Board PC (1981a) Biochemical genetics of glutathione S-transferase in man. Am J Hum Genet 33:36–43
Board PG (1981b) Gene deletion and partial deficiency of the glutathione S-transferase (ligandin) system in man. FEBS Lett 135:12–14
Chasseaud LF (1979) The role of glutathione S-transferases in the metabolism of chemical carcinogenes and other electrophilic agents. Adv Cancer Res 29:175–274
Comstock KE, Sanderson BJS, Claflin G, Henner WD (1990) GST1 gene deletion determined by polymerase chain reaction. Nucleic Acids Res 18:3670
Harada S, Abei M, Tanaka N, Agarwal DP, Goedde HW (1987) Liver glutathione S-transferase polymorphism in Japanese and its pharmacogenetic importance. Hum Genet 75:322–325
Lai HCJ, Qian B, Grove G, Chen-Pei DT (1988) Gene expression of rat glutathione S-transferases. Evidence for gene conversion in the evolution of the Yb multigene family. J Biol Chem 263:11389–11395
Laisney V, Nguyen van Cong, Gross MS, Frezal J (1984) Human genes for glutathione S-transferases. Hum Genet 68:221–227
Saiki RK, Golfand DH, Stoffel S, Scharf ST, Higuchi R, Horn GT, Mullis KB, Erlich HA (1988) Primer directed enzymatic amplification of DNA with a thermostabile DNA polymerase. Science 239:487–491
Seidegard J, Ronald WP, Miller DG (1986) A glutathione S-transferase in human leucocytes as a marker for susceptibility to lung cancer. Carcinogenesis 7:751–753
Seidegard J, Vorachek WR, Pero RW, Pearson WR (1988) Herditary differences in the expression of the human glutathione transferase active on trans-stilbene oxide are due to a gene deletion. Proc Natl Acad Sci USA 85:7293–7297
Seidegard J, Pero RW, Markowits MM, Roush G, Miller DG, Beattie EJ (1990) Isozyme of glutathione transferase (class Mu) as a marker for the susceptibility to lung cancer: a follow up study. Carcionogenesis 11:33–36
Strange RC, Faulder CG, Davis BA, Hume R, Brown JAH, Cotton W, Hopkinson DA (1984) The human glutathione S-transferases: studies of the tissue distribution and genetic variation of the GST1, GST2 and GST3 isozymes. Ann Hum Genet 48:11–20
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Harada, S., Misawa, S., Nakamura, T. et al. Detection of GST1 gene deletion by the polymerase chain reaction and its possible correlation with stomach cancer in Japanese. Hum Genet 90, 62–64 (1992). https://doi.org/10.1007/BF00210745
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DOI: https://doi.org/10.1007/BF00210745