Genetic architecture of mouse skin inflammation and tumour susceptibility

David A. Quigley, Minh D. To, Jesús Pérez-Losada, Facundo G. Pelorosso, Jian-Hua Mao, Hiroki Nagase, David G. Ginzinger and Allan Balmain ()
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David A. Quigley: Helen Diller Family Comprehensive Cancer Center,
Minh D. To: Helen Diller Family Comprehensive Cancer Center,
Jesús Pérez-Losada: Facultad de Medicina, Universidad de Salamanca, Campus Miguel de Unamuno s/n
Facundo G. Pelorosso: Helen Diller Family Comprehensive Cancer Center,
Jian-Hua Mao: Helen Diller Family Comprehensive Cancer Center,
Hiroki Nagase: Advanced Research Institute for the Sciences and Humanities, Nihon University
David G. Ginzinger: Helen Diller Family Comprehensive Cancer Center,
Allan Balmain: Helen Diller Family Comprehensive Cancer Center,

Nature, 2009, vol. 458, issue 7237, 505-508

Abstract: Susceptibility to skin cancer Systems genetics approaches are beginning to reveal how inherited genetic variants affect the structure and function of normal tissues, as well as individual susceptibility to diseases. A systems genetics study of skin tumour incidence, using crosses between two strains of mice one of which is susceptible and the other resistant to tumour development, has now been used to map genetic variants that contribute to skin cancer susceptibility. A comparison of gene expression in mutant mice with that in normal skin identifies gene expression motifs that contribute to tissue organization and various biological functions; key features emerging are a candidate master regulator of hair follicle fate, and a regulator of coordinated control of epidermal barrier function, inflammation and tumour susceptibility.

Date: 2009
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DOI: 10.1038/nature07683

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