P.J. Brooks, Ph.D., Acting Section Chief
National Institute on Alcohol Abuse and Alcoholism
National Institutes of Health
5625 Fishers Lane, Room 3S-24B:MSC 9412
Bethesda MD 20892-9412
telephone: +1 301.496.7920
fax: +1 301.480.2839
e-mail: pjbrooks@mail.nih.gov
Acting chief. Dr. Brooks joined LNG as a postdoctoral fellow in 1993, having previously trained with Donald Pfaff at the Rockefeller Institute. At LNG he developed a new line of research in DNA repair and human disease. After a strong review at BSC 2000, he was selected by a search committee and awarded a Tenure-Track Scientist position August, 2001.
Dr. Brooks was a member of the International Agency for Research on Cancer (IARC) Working Group that recently evaluated the carcinogenic risk of alcoholic beverages to humans, which concluded that drinking alcohol increases the risk of cancer of the upper aerodigestive tract, liver, colon and breast.
Mission Statement:
The major theme of research in the section of Molecular Neurobiology is DNA damage in relation to human disease, particularly neurological disease and cancer. The work of the section is divided into two interrelated projects.
The first project focuses on the mechanisms of neurological disease associated with DNA damage, with the specific goal of understanding the mechanistic basis of neurodegeneration in patients with the genetic disease xeroderma pigmentosum (XP), who lack the capacity to carry out a specific type of DNA repair called nucleotide excision repair (NER). Much of the work in this project is focused in a unique type of oxidative DNA lesion called a cyclopurine, including its effect on transcription, and other DNA processing enzymes.
A second project addresses the genotoxic effects of acetaldehyde, and the role of acetaldehyde derived DNA adducts in cancer development resulting from alcohol abuse. The emphasis in this project is on the structural basis of how acetaldehyde derived lesions interact with DNA processing enzymes such as RNA and DNA polymerases, as well as indemnification of the DNA repair pathways the protect the genome against acetaldehyde derived genotoxicity. We have found that the NER pathway is also the one of the major pathways in protecting against acetaldehyde derived DNA damage. This work is related to the mission of the LNG as a whole, since variation in the relevant DNA repair genes may affect susceptibility to alcohol-related cancers.
Cheryl Marietta, M.S.,
301.496.7921
cmarie@mail.nih.gov
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A Physiologist, assists Dr. Brooks in DNA repair assays, transfections and adduct measurements in cells and tissue culture.
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Tsu-Fan Cheng, Ph.D.,
301.496.7920
chengtsu@mail.nih.gov
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A postdoctoral fellow who obtained his Ph.D. from the State University of New York and Stony Brook. Within the Section on Molecular Neurobiology, he is working on the effects of DNA lesions on transcription by RNA polymerases.
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Selected Publications:
Jacob A. Theruvathu, Pawel Jaruga, Raghu G. Nath, Miral Dizdaroglu and PJ Brooks: Polyamines stimulate the formation of mutagenic 1,N2-propanodeoxyguanosine adducts from acetaldehyde. Nucleic Acids Research 2005;33(11):3513–20.
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Pawel Jaruga, Jacob Theruvathu, Miral Dizdaroglu and Philip J. Brooks: Complete release of (50S)-8,50-cyclo-20-deoxyadenosine from dinucleotides, oligodeoxynucleotides and DNA, and direct comparison of its levels in cellular DNA with other oxidatively induced DNA lesions. Nucleic Acids Research 2004;32(11) e87
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PJ Brooks: DNA repair in neural cells: basic science and clinical implications. Mutation Research 509 (2002) 93–108
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Kurt Randerath, Guo-Dong Zhou, Robert L. Somers, Jay H. Robbins and Philip J. Brooks: A 32P-Postlabeling Assay for the Oxidative DNA Lesion 8,5 -Cyclo-2 -deoxyadenosine in Mammalian Tissues. The Journal of Biological Chemistry 2001;276 (38):36051–7. [
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Philip J. Brooks, Dean S. Wise, David A. Berry, Joseph V. Kosmoskii, Michael J. Smerdoni, Robert L. Somers, Hugh Mackie, Alexander Y. Spoonde, Eric J. Ackerman, Katherine Coleman, Robert E. Tarone, and Jay H. Robbins: The Oxidative DNA Lesion 8,5'-(S)-Cyclo-2'-deoxyadenosine Is Repaired by the Nucleotide Excision Repair Pathway and Blocks Gene Expression in Mammalian Cells. The Journal of Biological Chemistry 2000;275(29):22355–62 [
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Updated: June 2007