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Article: Keratinocyte-specific Pten deficiency results in epidermal hyperplasia, accelerated hair follicle morphogenesis and tumor formation
Title | Keratinocyte-specific Pten deficiency results in epidermal hyperplasia, accelerated hair follicle morphogenesis and tumor formation |
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Authors | |
Issue Date | 2003 |
Citation | Cancer Research, 2003, v. 63, n. 3, p. 674-681 How to Cite? |
Abstract | PTEN is a tumor suppressor gene mutated in many human cancers. We used the Cre-loxP system to generate a keratinocyte-specific null mutation of Pten in mice (k5Ptenflox/flox mice). k5Ptenflox/flox mice exhibit wrinkled skin because of epidermal hyperplasia and hyperkeratosis and ruffled, shaggy, and curly hair. Histological examination revealed that skin morphogenesis is accelerated in k5Ptenflox/flox mice. Within 3 weeks of birth, 90% of k5Ptenflox/flox mice die of malnutrition possibly caused by hyperkeratosis of the esophagus. All k5Ptenflox/flox mice develop spontaneous tumors within 8.5 months of birth, and chemical treatment accelerates the onset of tumors. k5Ptenflox/flox keratinocytes are hyperproliferative and resistant to apoptosis and show increased activation of the Pten downstream signaling mediators Akt/protein kinase B (PKB) and extracellular signal-regulated kinase. Pten is thus an important regulator of normal development and oncogenesis in the skin. |
Persistent Identifier | http://hdl.handle.net/10722/292519 |
ISSN | 2023 Impact Factor: 12.5 2023 SCImago Journal Rankings: 3.468 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Suzuki, Akira | - |
dc.contributor.author | Itami, Satoshi | - |
dc.contributor.author | Ohishi, Minako | - |
dc.contributor.author | Hamada, Koichi | - |
dc.contributor.author | Inoue, Tae | - |
dc.contributor.author | Komazawa, Nobuyasu | - |
dc.contributor.author | Senoo, Haruki | - |
dc.contributor.author | Sasaki, Takehiko | - |
dc.contributor.author | Takeda, Junji | - |
dc.contributor.author | Manabe, Motomu | - |
dc.contributor.author | Mak, Tak Wah | - |
dc.contributor.author | Nakano, Toru | - |
dc.date.accessioned | 2020-11-17T14:56:39Z | - |
dc.date.available | 2020-11-17T14:56:39Z | - |
dc.date.issued | 2003 | - |
dc.identifier.citation | Cancer Research, 2003, v. 63, n. 3, p. 674-681 | - |
dc.identifier.issn | 0008-5472 | - |
dc.identifier.uri | http://hdl.handle.net/10722/292519 | - |
dc.description.abstract | PTEN is a tumor suppressor gene mutated in many human cancers. We used the Cre-loxP system to generate a keratinocyte-specific null mutation of Pten in mice (k5Ptenflox/flox mice). k5Ptenflox/flox mice exhibit wrinkled skin because of epidermal hyperplasia and hyperkeratosis and ruffled, shaggy, and curly hair. Histological examination revealed that skin morphogenesis is accelerated in k5Ptenflox/flox mice. Within 3 weeks of birth, 90% of k5Ptenflox/flox mice die of malnutrition possibly caused by hyperkeratosis of the esophagus. All k5Ptenflox/flox mice develop spontaneous tumors within 8.5 months of birth, and chemical treatment accelerates the onset of tumors. k5Ptenflox/flox keratinocytes are hyperproliferative and resistant to apoptosis and show increased activation of the Pten downstream signaling mediators Akt/protein kinase B (PKB) and extracellular signal-regulated kinase. Pten is thus an important regulator of normal development and oncogenesis in the skin. | - |
dc.language | eng | - |
dc.relation.ispartof | Cancer Research | - |
dc.title | Keratinocyte-specific Pten deficiency results in epidermal hyperplasia, accelerated hair follicle morphogenesis and tumor formation | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.pmid | 12566313 | - |
dc.identifier.scopus | eid_2-s2.0-0037309972 | - |
dc.identifier.volume | 63 | - |
dc.identifier.issue | 3 | - |
dc.identifier.spage | 674 | - |
dc.identifier.epage | 681 | - |
dc.identifier.isi | WOS:000180697700020 | - |
dc.identifier.issnl | 0008-5472 | - |