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Investigation of skin carcinogenesis in animals genetically selected for maximal or minimal acute inflammatory response homozygous for Slc11a1 R and S alleles.

Grant number: 10/01806-0
Support Opportunities:Scholarships in Brazil - Master
Effective date (Start): August 01, 2010
Effective date (End): May 31, 2012
Field of knowledge:Biological Sciences - Immunology - Immunogenetics
Principal Investigator:Marcelo de Franco
Grantee:Mariana Perlati dos Santos
Host Institution: Instituto Butantan. Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil


In an attempt to further elucidate the involvement of inflammation in carcinogenesis, genetically selected mice to develop an maximum (AIRmax) or minimal (AIRmin)acute inflammatory reaction are used in several studies that promote the induction of tumor initiation and progression in the skin. AIRmax mice are significantly more resistant to skin carcinogenesis than mice AIRmin. The gene solute carrier family 11a member 1 (Slc11a1) encodes a transmembrane protein involved in ion transport in the phagolysosomes of macrophages and neutrophils, and has an allelic polymorphism that modulates the activity of these cells, and susceptibility to infections and autoimmune diseases. The existence of disequilibrium in frequency of alleles R and S of the Slc11a1 gene in animals AIRmax and AIRmin allowed establishing homozygous sublineages for these alleles, which were produced by Slc11a1 genotype-assisted mating. This study is therefore to investigate the skin carcinogenesis induced by DMBA in sublineages agent AIRmaxSS, AIRmaxRR, AIRminSS, AIRminRR, evaluating the genetic, cellular and physiological mechanisms involved in disease progression.

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