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Article: Hyperplasia and carcinomas in Pten-deficient mice and reduced PTEN protein in human bladder cancer patients

TitleHyperplasia and carcinomas in Pten-deficient mice and reduced PTEN protein in human bladder cancer patients
Authors
Issue Date2006
Citation
Cancer Research, 2006, v. 66, n. 17, p. 8389-8396 How to Cite?
AbstractPTEN is a tumor suppressor gene mutated in many human cancers. We used the Cre-loxP system to generate an urothelium-specific null mutation of Pten in mice [FabpCrePtenflox/flox (FPtenflox/flox) mice]. Histologic examination revealed that all FPtenflox/flox mice exhibited urothelial hyperplasia in which component cells showed enlarged nuclei and increased cell size. With time, 10% of FPtenflox/flox mice spontaneously developed pedicellate papillary transitional cell carcinomas (TCC). This type of tumor also arose in FPtenflox/flox mice treated with the chemical carcinogen N-butyl-N-(4-hydroxybutyl) nitrosamine. EPten flox/flox urothelial cells were hyperproliferative and showed increased activation of the survival signaling molecules Akt and extracellular signal-regulated kinase. In humans, 53% of primary bladder cancer patients exhibited decreased or absent expression of PTEN protein in either the cytoplasm or nucleus of tumor cells. In early bladder cancers, PTEN expression was repressed in 42% of superficial papillary TCC but in only 8% of cases of carcinoma in situ (CIS). In advanced bladder cancers, PTEN protein was significantly reduced (particularly in the nucleus) in 94% of cases, and this decrease in PTEN correlated with disease stage and grade. Thus, PTEN deficiency may contribute to bladder cancer both by initiating superficial papillary TCC and by promoting the progression of CIS to advanced invasive and metastatic forms. ©2006 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/292588
ISSN
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.468
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTsuruta, Hiroshi-
dc.contributor.authorKishimoto, Hiroyuki-
dc.contributor.authorSasaki, Takehiko-
dc.contributor.authorHorie, Yasuo-
dc.contributor.authorNatsui, Miyuki-
dc.contributor.authorShibata, Yoshiko-
dc.contributor.authorHamada, Koichi-
dc.contributor.authorYajima, Nobuyuki-
dc.contributor.authorKawahara, Koichi-
dc.contributor.authorSasaki, Masato-
dc.contributor.authorTsuchiya, Norihiko-
dc.contributor.authorEnomoto, Katsuhiko-
dc.contributor.authorMak, Tak Wah-
dc.contributor.authorNakano, Toru-
dc.contributor.authorHabuchi, Tomonori-
dc.contributor.authorSuzuki, Akira-
dc.date.accessioned2020-11-17T14:56:48Z-
dc.date.available2020-11-17T14:56:48Z-
dc.date.issued2006-
dc.identifier.citationCancer Research, 2006, v. 66, n. 17, p. 8389-8396-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/292588-
dc.description.abstractPTEN is a tumor suppressor gene mutated in many human cancers. We used the Cre-loxP system to generate an urothelium-specific null mutation of Pten in mice [FabpCrePtenflox/flox (FPtenflox/flox) mice]. Histologic examination revealed that all FPtenflox/flox mice exhibited urothelial hyperplasia in which component cells showed enlarged nuclei and increased cell size. With time, 10% of FPtenflox/flox mice spontaneously developed pedicellate papillary transitional cell carcinomas (TCC). This type of tumor also arose in FPtenflox/flox mice treated with the chemical carcinogen N-butyl-N-(4-hydroxybutyl) nitrosamine. EPten flox/flox urothelial cells were hyperproliferative and showed increased activation of the survival signaling molecules Akt and extracellular signal-regulated kinase. In humans, 53% of primary bladder cancer patients exhibited decreased or absent expression of PTEN protein in either the cytoplasm or nucleus of tumor cells. In early bladder cancers, PTEN expression was repressed in 42% of superficial papillary TCC but in only 8% of cases of carcinoma in situ (CIS). In advanced bladder cancers, PTEN protein was significantly reduced (particularly in the nucleus) in 94% of cases, and this decrease in PTEN correlated with disease stage and grade. Thus, PTEN deficiency may contribute to bladder cancer both by initiating superficial papillary TCC and by promoting the progression of CIS to advanced invasive and metastatic forms. ©2006 American Association for Cancer Research.-
dc.languageeng-
dc.relation.ispartofCancer Research-
dc.titleHyperplasia and carcinomas in Pten-deficient mice and reduced PTEN protein in human bladder cancer patients-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-05-4627-
dc.identifier.pmid16951148-
dc.identifier.scopuseid_2-s2.0-33748999833-
dc.identifier.volume66-
dc.identifier.issue17-
dc.identifier.spage8389-
dc.identifier.epage8396-
dc.identifier.isiWOS:000240329400013-
dc.identifier.issnl0008-5472-

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