- Full (HTML) - Full (PDF) - Related EHP Articles - PubMed:Related Articles - PubMed:Citation - Cited in PMC - Purchase This Issue

-Aminolevulinic Acid Dehydratase Polymorphism and Risk of Brain Tumors in Adults

Preetha Rajaraman,¹ Brian S. Schwartz,² Nathaniel Rothman,¹ Meredith Yeager,³ Howard A. Fine,⁴ William R. Shapiro,⁵ Robert G. Selker,⁶ Peter M. Black,⁷ and Peter D. Inskip¹

¹Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA; ²Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA; ³Core Genotyping Facility, and ⁴Neuro-oncology Branch, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA; ⁵Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona, USA; ⁶Western Pennsylvania Hospital, Pittsburgh, Pennsylvania, USA; ⁷Brigham and Women's Hospital, Boston, Massachusetts, USA

Abstract
The enzyme -aminolevulinic acid dehydratase (ALAD) , which catalyzes the second step of heme synthesis, can be inhibited by several chemicals, including lead, a potential risk factor for brain tumors, particularly meningioma. In this study we examined whether the ALAD G177C polymorphism in the gene coding for ALAD is associated with risk of intracranial tumors of the brain and nervous system. We use data from a case-control study with 782 incident brain tumor cases and 799 controls frequency matched on hospital, age, sex, race/ethnicity, and residential proximity to the hospital. Blood samples were drawn and DNA subsequently sent for genotyping for 73% of subjects. ALAD genotype was determined for 94% of these samples (355 glioma, 151 meningioma, 67 acoustic neuroma, and 505 controls) . Having one or more copy of the ALAD2 allele was associated with increased risk for meningioma [odds ratio (OR) = 1.6 ; 95% confidence interval (CI) , 1.0-2.6], with the association appearing stronger in males (OR = 3.5 ; 95% CI, 1.3-9.2) than in females (OR = 1.2 ; 95% CI, 0.7-2.2) . No increased risk associated with the ALAD2 variant was observed for glioma or acoustic neuroma. These findings suggest that the ALAD2 allele may increase genetic susceptibility to meningioma. Key words: ALAD, brain, case-control, meningioma, polymorphism, tumor. Environ Health Perspect 113:1209-1211 (2005) . doi:10.1289/ehp.7986 available via http://dx.doi.org/ [Online 10 May 2005]

Address correspondence to P. Rajaraman, REB, National Cancer Institute, NIH, DHHS, 6120 Executive Blvd., EPS Room 7085, Bethesda, MD 20892-7238 USA. Telephone: (301) 496-8847. Fax: (301) 402-0207. E-mail: rajarama@mail.nih.gov

The authors declare they have no competing financial interests.

Received 2 February 2005 ; accepted 10 May 2005.