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Article: Pten deficiency in melanocytes results in resistance to hair graying and susceptibility to carcinogen-induced melanomagenesis

TitlePten deficiency in melanocytes results in resistance to hair graying and susceptibility to carcinogen-induced melanomagenesis
Authors
Issue Date2008
Citation
Cancer Research, 2008, v. 68, n. 14, p. 5760-5768 How to Cite?
AbstractPhosphate and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor gene inactivated in numerous sporadic cancers, including melanomas. To analyze Pten functions in melanocytes, we used the Cre-loxP system to delete Pten specifically in murine pigment-producing cells and generated DctCrePtenflox/flox mice. Half of DctCrePtenflox/flox mice died shortly after birth with enlargements of the cerebral cortex and hippocampus. Melanocytes were increased in the dermis of perinatal DctCrePtenflox/flox mice. When the mutants were subjected to repeated depilations, melanocyte stem cells in the bulge of the hair follicle resisted exhaustion and the mice were protected against hair graying. Although spontaneous melanomas did not form in DctCrePtenflox/flox mice, large nevi and melanomas developed after carcinogen exposure. DctCrePten flox/flox melanocytes were increased in size and exhibited heightened activation of Akt and extracellular signal-regulated kinases, increased expression of Bcl-2, and decreased expression of p27Kip1. Our results show that Pten is important for the maintenance of melanocyte stem cells and the suppression of melanomagenesis. ©2008 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/291846
ISSN
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.468
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorInoue-Narita, Tae-
dc.contributor.authorHamada, Koichi-
dc.contributor.authorSasaki, Takehiko-
dc.contributor.authorHatakeyama, Sachiko-
dc.contributor.authorFujita, Sachiko-
dc.contributor.authorKawahara, Kohichi-
dc.contributor.authorSasaki, Masato-
dc.contributor.authorKishimoto, Hiroyuki-
dc.contributor.authorEguchi, Satoshi-
dc.contributor.authorKojima, Itaru-
dc.contributor.authorBeermann, Friedrich-
dc.contributor.authorKimura, Tetsunori-
dc.contributor.authorOsawa, Masatake-
dc.contributor.authorItami, Satoshi-
dc.contributor.authorMak, Tak Wah-
dc.contributor.authorNakano, Toru-
dc.contributor.authorManabe, Motomu-
dc.contributor.authorSuzuki, Akira-
dc.date.accessioned2020-11-17T14:55:14Z-
dc.date.available2020-11-17T14:55:14Z-
dc.date.issued2008-
dc.identifier.citationCancer Research, 2008, v. 68, n. 14, p. 5760-5768-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/291846-
dc.description.abstractPhosphate and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor gene inactivated in numerous sporadic cancers, including melanomas. To analyze Pten functions in melanocytes, we used the Cre-loxP system to delete Pten specifically in murine pigment-producing cells and generated DctCrePtenflox/flox mice. Half of DctCrePtenflox/flox mice died shortly after birth with enlargements of the cerebral cortex and hippocampus. Melanocytes were increased in the dermis of perinatal DctCrePtenflox/flox mice. When the mutants were subjected to repeated depilations, melanocyte stem cells in the bulge of the hair follicle resisted exhaustion and the mice were protected against hair graying. Although spontaneous melanomas did not form in DctCrePtenflox/flox mice, large nevi and melanomas developed after carcinogen exposure. DctCrePten flox/flox melanocytes were increased in size and exhibited heightened activation of Akt and extracellular signal-regulated kinases, increased expression of Bcl-2, and decreased expression of p27Kip1. Our results show that Pten is important for the maintenance of melanocyte stem cells and the suppression of melanomagenesis. ©2008 American Association for Cancer Research.-
dc.languageeng-
dc.relation.ispartofCancer Research-
dc.titlePten deficiency in melanocytes results in resistance to hair graying and susceptibility to carcinogen-induced melanomagenesis-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-08-0889-
dc.identifier.pmid18632629-
dc.identifier.scopuseid_2-s2.0-48649110016-
dc.identifier.volume68-
dc.identifier.issue14-
dc.identifier.spage5760-
dc.identifier.epage5768-
dc.identifier.isiWOS:000257768300033-
dc.identifier.issnl0008-5472-

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