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Cancer Genes and Genomics

Microarray Analysis of Bleomycin-Exposed Lymphoblastoid Cells for Identifying Cancer Susceptibility Genes

¹ Section Tumor Biology, Department of Otolaryngology/Head-Neck Surgery, ² Department of Pediatric Oncology/Hematology, ³ Department of Medical Oncology, and ⁴ Microarray Core Facility, VU University Medical Center, Amsterdam, the Netherlands

Requests for reprints: Boudewijn J.M. Braakhuis, Section Tumor Biology, Department of Otolaryngology/Head-Neck Surgery, VU University Medical Center, P.O. Box 7057, 1007 MB Amsterdam, the Netherlands. Phone: 31-20-444-0905; Fax: 31-20-444-3688. E-mail: bjm.braakhuis{at}vumc.nl

The uncovering of genes involved in susceptibility to the sporadic cancer types is a great challenge. It is well established that the way in which an individual deals with DNA damage is related to the chance to develop cancer. Mutagen sensitivity is a phenotype that reflects an individual's susceptibility to the major sporadic cancer types, including colon, lung, and head and neck cancer. A standard test for mutagen sensitivity is measuring the number of chromatid breaks in lymphocytes after exposure to bleomycin. The aim of the present study was to search for the pathways involved in mutagen sensitivity. Lymphoblastoid cell lines of seven individuals with low mutagen sensitivity were compared with seven individuals with a high score. RNA was isolated from cells exposed to bleomycin (4 hours) and from unexposed cells. Microarray analysis (19K) was used to compare gene expression of insensitive and sensitive cells. The profile of most altered genes after bleomycin exposure, analyzed in all 14 cell lines, included relatively many genes involved in biological processes, such as cell growth and/or maintenance, proliferation, and regulation of cell cycle, as well as some genes involved in DNA repair. When comparing the insensitive and sensitive individuals, other differentially expressed genes were found that are involved in signal transduction and cell growth and/or maintenance (e.g., BUB1 and DUSP4). This difference in expression profiles between mutagen-sensitive and mutagen-insensitive individuals justifies further studies aimed at elucidating the genes responsible for the development of sporadic cancers. (Mol Cancer Res 2006;4(2):71–7)

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				X. Wu, J. Gu, and M. R. Spitz Mutagen Sensitivity: A Genetic Predisposition Factor for Cancer Cancer Res., April 15, 2007; 67(8): 3493 - 3495. [Abstract] [Full Text] [PDF]