NDLI: DNA-lesion mapping in mammalian cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Besaratinia, Ahmad Pfeifer, Gerd P.
Description	Country affiliation: United States Author Affiliation: Besaratinia A ( Division of Biology, Beckman Research Institute of the City of Hope National Medical Center, Duarte, CA 91010, USA. ania@coh.org)
Abstract	Formation of DNA damage is a crucial event in carcinogenesis. Irreparable DNA lesions have the potential to cause mispairing during DNA replication, thereby giving rise to mutations. Critically important mutations in cancer-related genes, i.e., oncogenes and tumor suppressor genes, are key contributors to carcinogenesis. Theoretically, co-localization(s) of persistent DNA lesions and mutational hotspots in cancer-relevant genes can be used for causality inference. The inferred causality can be validated if a suspected carcinogen can similarly produce corresponding patterns of DNA damage and mutagenesis in vitro and/or in vivo. DNA-lesion footprinting (mapping) in conjunction with mutagenicity analysis is used for investigating cancer etiology. Ligation-mediated polymerase chain reaction (LM-PCR) is a versatile DNA-lesion footprinting technique, which enables sensitive and specific detection of DNA damage, at the level of nucleotide resolution, in genomic DNA. Here, we describe an updated protocol for LM-PCR analysis of the mammalian genome. This protocol can routinely be used for DNA-lesion footprinting of a variety of chemical and/or physical carcinogens in mammalian cells.
File Format	HTM / HTML
ISSN	10462023
e-ISSN	10959130
DOI	10.1016/j.ymeth.2009.02.008
Journal	Methods
Issue Number	1
Volume Number	48
Language	English
Publisher	Elsevier
Publisher Date	2009-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Life sciences, Biochemistry Cells Dna Damage Dna Footprinting Dna Ligases Metabolism Polymerase Chain Reaction Animals Base Pairing Carcinogens Toxicity Cell Transformation, Neoplastic Chemically Induced Genetics Dna Adducts Dna Mutational Analysis Dna Primers Genes, P53 Genome, Human Mammals Mutagenesis Mutation Drug Effects Nucleic Acid Amplification Techniques Pyrimidine Dimers Radiation Effects Reproducibility Of Results Sensitivity And Specificity Sequence Analysis, Dna Templates, Genetic Ultraviolet Rays Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Molecular Biology

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Differential replication of a single, UV-induced lesion in the leading or lagging strand by a human cell extract: fork uncoupling or gap formation.

Influence of cytosine methylation on ultraviolet-induced cyclobutane pyrimidine dimer formation in genomic DNA.

DNA-lesion mapping in mammalian cells.

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Solution structure of a DNA decamer duplex containing the stable 3′ T⋅G base pair of the pyrimidine(6–4)pyrimidone photoproduct [(6–4) adduct]: Implications for the highly specific 3′ T → C transition of the (6–4) adduct

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