Germ-line variants in methyl-group metabolism genes and susceptibility to DNA methylation in normal tissues and human primary tumors

Cancer Research

Volumn 62, Issue 15, 2002, Pages 4519-4524

  Paz, Maria F ^a   Avila, Sonia ^a   Fraga, Mario F ^a   Pollan, Marina ^b   Capella, Gabriel ^c   Peinado, Miquel Angel ^c   Sanchez Cespedes, Montserrat ^a   Herman, James G ^d   Esteller, Manel ^a  

^a Centro Nacional de Investigaciones Oncológicas   (Spain)

^b CARLOS III INSTITUTE OF HEALTH   (Spain)

^c Institut de Recerca Oncologica   (Spain)

^d JOHNS HOPKINS UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

5 METHYLCYTOSINE; 5,10 METHYLENETETRAHYDROFOLATE REDUCTASE (FADH2); CYSTATHIONINE BETA SYNTHASE; DNA; METHIONINE SYNTHASE;

ALLELE; ARTICLE; CANCER SUSCEPTIBILITY; COLORECTAL CARCINOMA; CPG ISLAND; DISEASE ASSOCIATION; DNA METHYLATION; GENETIC POLYMORPHISM; GENETIC SUSCEPTIBILITY; GENOME; GENOTYPE; HUMAN; HUMAN TISSUE; MAJOR CLINICAL STUDY; PRIORITY JOURNAL; TUMOR SUPPRESSOR GENE;

5-METHYLCYTOSINE; 5-METHYLTETRAHYDROFOLATE-HOMOCYSTEINE S-METHYLTRANSFERASE; ADENOCARCINOMA; BREAST NEOPLASMS; COLORECTAL NEOPLASMS; CPG ISLANDS; CYSTATHIONINE BETA-SYNTHASE; CYTOSINE; DNA METHYLATION; DNA, NEOPLASM; GENETIC PREDISPOSITION TO DISEASE; GERM-LINE MUTATION; HUMANS; LUNG NEOPLASMS; METHYLENETETRAHYDROFOLATE REDUCTASE (NADPH2); NEOPLASMS; OXIDOREDUCTASES ACTING ON CH-NH GROUP DONORS;

EID: 0036682379     PISSN: 00085472     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (48)

1. Cancer epigenetics comes of age
2. Aberrant patterns of DNA methylation, chromatin formation and gene expression in cancer
3. Cancer as an epigenetic disease: DNA methylation and chromatin alterations in human tumours
4. DNA hypomethylation and cancer
5. A gene hypermethylation profile of human cancer
6. Aberrant CpG-island methylation has non-random and tumour-type-specific patterns
7. Sp1 sites in the mouse APRT gene promoter are required to prevent methylation of the CpG island
8. Sp1 elements protect a CpG island from de novo methylation
9. Transcription factor Spl is essential for early development but dispensable for cell growth and differentiation
10. Mapping patterns of CpG island methylation in normal and neoplastic cells implicates both upstream and downstream regions in de novo methylation
11. Age-related hypermethylation of the 5′ region of MLH1 in normal colonic mucosa is associated with microsatellite-unstable colorectal cancer development
12. The DNA methyltransferases of mammals
13. DNA methylation, methyltransferases, and cancer
14. Mutations in ATRX, encoding a SWI/SNF-like protein, cause diverse changes in the pattern of DNA methylation
15. CpG methylation is maintained in human cancer cells lacking DNMT1
16. Hypomethylation of hepatic nuclear DNA in rats fed with a carcinogenic methyl-deficient diet
17. Methionine metabolism and cancer
18. Choline deficiency and chemical carcinogenesis
19. Methyl groups in carcinogenesis: Effects on DNA methylation and gene expression
20. A candidate genetic risk factor for vascular disease: A common mutation in methylenetetrahydrofolate reductase
21. A second common mutation in the methylenetetrahydrofolate reductase gene: An additional risk factor for neural-tube defects?
22. Methionine synthase D919G polymorphism is a significant but modest determinant of circulating homocysteine concentrations
23. High prevalence of a mutation in the cystathionine β-synthase gene
24. A methylenetetrahydrofolate reductase polymorphism, and the risk of colorectal cancer
25. Methyl group metabolism gene polymorphisms and susceptibility to prostatic carcinoma
26. Polymorphisms of 5, 10-methylenetetrahydrofolate reductase and risk of gastric cancer in a Chinese population: A case-control study
27. Baylin a novel PCR assay for methylation status of CpG islands
28. DNA methylation patterns in hereditary human cancers mimic sporadic tumorigenesis
29. Rapid quantification of DNA methylation by high performance capillary electrophoresis
30. Haplotype analysis in population-based association studies
31. 5, 10-Methylenetetrahydrofolate reductase gene variants and congenital anomalies: A HuGE review
32. Folate, homocysteine, and neural tube defects: An overview
33. MTHFR 677 C→T mutation: A predictor of early-onset coronary artery disease risk
34. Methylation of the estrogen receptor gene is associated with aging and atherosclerosis in the cardiovascular system
35. Mutations in the gene encoding methyl-CpG-binding protein 2 cause Rett syndrome
36. Mice deficient in methylenetetrahydrofolate reductase exhibit hyperhomocysteinemia and decreased methylation capacity, with neuropathology and aortic lipid deposition
37. Genomic DNA hypomethylation, a characteristic of most cancers, is present in peripheral leukocytes of individuals who are homozygous for the C677T polymorphism in the methylenetetrahydrofolate reductase gene
38. Polymorphisms and colorectal tumor risk
39. Polymorphism of methylenetetrahydrofolate reductase and risk of lung cancer: A case control study
40. Germ line polymorphisms in cytochrome-P450 IA1 (C4887 CYPIA1) and methylenetetrahydrofolate reductase (MTHFR) genes and endometrial cancer susceptibility
41. Methylenetetrahydrofolate reductase (MTHFR) polymorphisms and risk of molecularly defined subtypes of childhood acute leukemia
42. Defects in human methionine synthase in cblG patients
43. Human methionine synthase: Cdna cloning and identification of mutations in patients of the cblG complementation group of folate/cobalamin disorders
44. A polymorphism of the methionine synthase gene: Association with plasma folate, vitamin B 12, homocyst(e)ine, and colorectal cancer risk
45. Reduced availability of endogenously synthesized methionine for S-adenosylmethionine formation in methionine-dependent cancer cells
46. Senescence of nickel-transformed cells by an X chromosome: Possible epigenetic control
47. Dietary selenium and arsenic affect DNA methylation in vitro in Caco-2 cells and in vivo in rat liver and colon
48. Methyl group deficiency in hepatocarcinogenesis