The methionine synthase polymorphism D919G alters susceptibility to primary central nervous system lymphoma

Linnebank, Michael; Schmidt, Stephan; Kölsch, Heike; Linnebank, Anja; Heun, Reinhard; Schmidt-Wolf, I.; Glasmacher, Axel; Fließbach, Klaus; Klockgether, Thomas; Schlegel, Uwe; Pels, Hendrik

doi:10.1038/sj.bjc.6601777

Cited by 39 publications

(34 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Transforming growth factor-b1 polymorphisms were confirmed by direct sequencing. The frequencies of the variant alleles were comparable with those reported in other studies (Hu et al, 2001;McDermott et al, 2001;Lebailly et al, 2002;Quarmby et al, 2003;Johnson et al, 2004;Linnebank et al, 2004), and all SNPs were in Hardy -Weinberg equilibrium (Table 4).…”

Section: Genetic Association Between Genotype and Phenotypesupporting

confidence: 87%

“…DNA was extracted from the buccal samples using the QIAamp DNA mini kit (QIAGEN GmbH, Germany), using the standard manufacturers' protocol. DNA was PCR amplified and analysed for QTG restriction fragment length polymorphisms using published PCR primers and PCR conditions, and restriction enzymes: TGFb1 (C-509T) (Quarmby et al, 2003); X-ray repair cross-complementing 1 (XRCC1; R399Q) and apurinic/apyrimidinic endonuclease (APE-1; D126E) (Hu et al, 2001); dihydrofolate reductase (DHFR; 15 bp intron 1 deletion) (Johnson et al, 2004); the CX3CR1 (G745A) fractalkine receptor (McDermott et al, 2001); epoxide hydrolase (Hyl-1; Y113H) (Lebailly et al, 2002); and methionine synthetase (MS; A2756G) and methylenetetrahydrofolate reductase (MTHFR; C667T) (Linnebank et al, 2004).…”

Section: Genetics Of Late Radiotherapy Damagementioning

confidence: 99%

“…The genes and corresponding SNP were chosen because XRCC1 (R399Q) and APE-1 (D126E) have been implicated in DNA repair (Hu et al, 2001;Chang-Claude et al, 2005;De Ruyck et al, 2005), TGFb1 (C-509T) and CX3CR1 (G745A) have been implicated in inflammation and fibrosis (Zugmaier et al, 1991;Randall and Coggle, 1995;Anscher et al, 1997;Li et al, 1999;Martin et al, 2000;McDermott et al, 2001;Gauldie et al, 2003), MTHFR (C667T), MS (A2756G) and DHFR (19 bp del intron 1) involved in folate metabolism (Johnson et al, 2004;Linnebank et al, 2004), epoxide hydrolase (Hyl1 Y113H) implicated in oxidative stress (Lebailly et al, 2002), and XRCC1 (R399Q) have been associated with susceptibility to breast cancer (Moullan et al, 2003). Additionally, several gene polymorphism have previously been implicated in late radiation-induced tissue damage (Awad et al, 1988;El-Gamel et al, 1999;Grainger et al, 1999;Quarmby et al, 2003;Andreassen et al, 2005;De Ruyck et al, 2005Brem et al, 2006), and TGFb1 and Hyl1 are induced following exposure to ionising radiation (Anscher et al, 1997;Martin et al, 1997).…”

Section: Genetic Association Between Genotype and Phenotypementioning

confidence: 99%

See 2 more Smart Citations

The late radiotherapy normal tissue injury phenotypes of telangiectasia, fibrosis and atrophy in breast cancer patients have distinct genotype-dependent causes

et al. 2007

View full text Add to dashboard Cite

The relationship between late normal tissue radiation injury phenotypes in 167 breast cancer patients treated with radiotherapy and: (i) radiotherapy dose (boost); (ii) an early acute radiation reaction and (iii) genetic background was examined. Patients were genotyped at single nucleotide polymorphisms (SNPs) in eight candidate genes. An early acute reaction to radiation and/or the inheritance of the transforming growth factor-b1 (TGFb1 À509T) SNP contributed to the risk of fibrosis. In contrast, an additional 15 Gy electron boost and/or the inheritance of X-ray repair cross-complementing 1 (XRCC1) (R399Q) SNP contributed to the risk of telangiectasia. Although fibrosis, telangiectasia and atrophy, all contribute to late radiation injury, the data suggest that they have distinct underlying genetic and radiobiological causes. Fibrosis risk is associated with an inflammatory response (an acute reaction and/ or TGFb1), whereas telangiectasia is associated with vascular endothelial cell damage (boost and/or XRCC1). Atrophy is associated with an acute response, but the genetic predisposing factors that determine the risk of an acute response or atrophy have yet to be identified. A combined analysis of two UK breast cancer patient studies shows that 8% of patients are homozygous (TT) for the TGFb1 (C-509T) variant allele and have a 15-fold increased risk of fibrosis following radiotherapy (95% confidence interval: 3.76 -60.3; P ¼ 0.000003) compared with (CC) homozygotes.

show abstract

Section: Genetic Association Between Genotype and Phenotypesupporting

confidence: 87%

Section: Genetics Of Late Radiotherapy Damagementioning

confidence: 99%

Section: Genetic Association Between Genotype and Phenotypementioning

confidence: 99%

See 1 more Smart Citation

The late radiotherapy normal tissue injury phenotypes of telangiectasia, fibrosis and atrophy in breast cancer patients have distinct genotype-dependent causes

et al. 2007

View full text Add to dashboard Cite

show abstract

“…MTR catalyzes the remethylation of homocysteine to methionine. The Gly allele of a SNP in the MTR gene (MTR 2756A>G, Asp919Gly), associated with lower homocysteine levels than the Asp allele, was inversely associated with lymphoma subtypes in Caucasians [24][25][26] and positively associated with NHL in another Caucasian study 18 and in an Asian population.…”

mentioning

confidence: 94%

Genetic susceptibility to lymphoma

Skibola¹,

Curry²,

Nieters³

2007

Haematologica

126

109

View full text Add to dashboard Cite

Genetic susceptibility studies of lymphoma may serve to identify at risk populations and clarify important disease mechanisms. This review considered all studies published through October 2006 on the contribution of genetic polymorphisms in the risk of lymphoma. Numerous studies implicate the role of genetic variants that promote B-cell survival and growth with increased risk of lymphoma. Several reports including a large pooled study by InterLymph, an international consortium of non-Hodgkin lymphoma (NHL) case-control studies, found positive associations between variant alleles in TNF -308G>A and IL10 -3575T>A genes and risk of diffuse large B-cell lymphoma. Four studies reported positive associations between a GSTT1 deletion and risk of Hodgkin and non-Hodgkin lymphoma. Genetic studies of folate-metabolizing genes implicate folate in NHL risk, but further studies that include folate and alcohol intakes are needed. Links between NHL and genes involved in energy regulation and hormone production and metabolism may provide insights into novel mechanisms implicating neuro-and endocrine-immune cross-talk with lymphomagenesis. However, this links will need replication in larger populations. Numerous studies suggest that common genetic variants with low penetrance influence lymphoma risk, though replication studies will be needed to eliminate false positive associations.

show abstract

“…PCNSL is known to be associated with immunodeficiency, for example, due to the acquired immunodeficiency syndrome (AIDS) or to long-term immunosuppressive therapy [2,3]. In immunocompetent patients, an association of PCNSL with the germline genetic variant methyltetrahydrofolate homocysteine Smethyltransferase (MTR) c.2756A>G (p.D919G) has been reported [4].…”

Section: Introductionmentioning

confidence: 99%

Primary CNS lymphoma and HLA class I and II alleles in a German cohort of immunocompetent patients

Kurzwelly

Müller²,

Korfel

et al. 2008

J Neurooncol

View full text Add to dashboard Cite

Human leukocyte antigens (HLA) are involved in the regulation of immune response to infection and in malignant transformation. Several HLA alleles are associated with immunological or malignant diseases. The aim of the present study was to evaluate a potential association of HLA class I and II alleles with primary central nervous system lymphoma (PCNSL) in immunocompetent patients. We therefore analyzed particular HLA-A, HLA-B and HLA-DRB1 alleles in 82 PCNSL patients and compared the data to those in 327 population controls. No significant difference between these two groups was found using Pearson's chi(2) test. These data do not support the hypothesis that HLA alleles play a major role in the pathogenesis of PCNSL.

show abstract

The methionine synthase polymorphism D919G alters susceptibility to primary central nervous system lymphoma

Cited by 39 publications

References 17 publications

The late radiotherapy normal tissue injury phenotypes of telangiectasia, fibrosis and atrophy in breast cancer patients have distinct genotype-dependent causes

The late radiotherapy normal tissue injury phenotypes of telangiectasia, fibrosis and atrophy in breast cancer patients have distinct genotype-dependent causes

Genetic susceptibility to lymphoma

Primary CNS lymphoma and HLA class I and II alleles in a German cohort of immunocompetent patients

Contact Info

Product

Resources

About