Nucleotide excision repair in aging & cancer

Leiden Repository

Nucleotide excision repair in aging & cancer

Title: Nucleotide excision repair in aging & cancer
Author: Melis, Joost
Publisher: Department of Toxicogenetica, Faculty of Medicine / Leiden University Medical Center (LUMC) Leiden University
Issue Date: 2012-11-06
Keywords: Nucleotide Excision Repair
Carcinogen identification
DNA damage
DNA repair
Gene expression
Abstract: DNA damage, mutations and genomic instability are established driving forces of cancer and other age-related diseases. Mutations in tumor suppressor genes and oncogenes are very frequently found in tumors and genomic instability is the most common enabling characteristic of cancer. Aging is also believed to be enabled, amongst others, by genomic instability. DNA repair pathways, like the nucleotide excision repair (NER) pathway and cell cycle control (e.g. p53-dependent) processes are therefore vital to organisms, since these processes counteract or prevent genomic instability, and are thought to underlie, when affected, aging and age-related diseases like cancer. To unravel the functions, mechanisms and pathways involved in the onset of aging and age-related diseases we have investigated several mouse models deficient in either DNA repair (NER) capacity (Chapter 3, 4), cell cycle control (p53) (Chapter 6) or both (Chapter 5), and compared this to a wild type situation (Chapter 2). The use of mouse models enabled us to investigate cancer and aging in a controlled environment, minimizing possible confounding factors. Additionally, the mouse models can be useful as an alternative tool to identify genotoxic and non-genotoxic carcinogens that can be harmful to the society and the environment (Chapter 5).
Description: Promotores: Harry van Steeg, Leon Mullenders, Co-promotor: Mirjam Luijten
With summary in Dutch
Faculty: LUMC
Citation: Melis, J.P.M., 2012, Doctoral thesis, Leiden University
ISBN: 9789081943413

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