@article{oai:air.repo.nii.ac.jp:00001618,
 author = {YAMAKAWA, Takehiro and INOUE-NARITA, Tae and TSUDA, Masaaki and HATAKEYAMA, Sachiko and FUJITA, Sachiko and SASAKI, Takehiko and SUZUKI, Akira and MANABE, Motomu},
 issue = {1},
 journal = {秋田医学},
 month = {Jun},
 note = {PTEN is a tumor suppressor gene that is mutated in many human sporadic cancers and in hereditary tumor susceptibility disorders such as Cowden disease. We have previously reported that keratinocyte-specific heterozygous Pten-deficient mice (K5CrePtenflox/+ mice) displayed enhanced susceptibility to carcinogenesis of the skin. Accordingly, to clarify whether the selective inhibition of phosphoinositide 3-kinase (PI3K) isoforms rescues the phenotypes of K5CrePtenflox/+ mice, we generated mice simultaneously lacking (PI3K) isoforms (p85α , p110α , p110δ or p110γ ) and Pten. Consequently, it was shown that heterozygous p110α deficiency (p110α +/−) and homozygous p110 deficiency (p110γ −/−) significantly rescued susceptibility to spontaneous carcinogenesis of the skin in K5CrePtenflox/+ mice. The present study sheds light on the possible role of p110α and p110γ in carcinogenesis of the skin ; thus providing new insights into a chemoprevention of squamous cell carcinoma.},
 pages = {19--23},
 title = {SUPPRESSION OF SPONTANEOUS CARCINOGENESIS IN KERATINOCYTE-SPECIFIC PTEN-DEFICIENT MICE WITH SELECTIVE INHIBITION OF PI3K ISOFORMS},
 volume = {36},
 year = {2009}
}