PTEN Mouse Models of Cancer Initiation and Progression.
Cold Spring Harb Perspect Med
; 10(2)2020 02 03.
Article
en En
| MEDLINE
| ID: mdl-31570383
ABSTRACT
Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is one of the most frequently mutated, deleted, and functionally inactivated tumor suppressor genes in human cancer. PTEN is found mutated both somatically and in the germline of patients with PTEN hamartoma tumor syndrome (PHTS). PTEN encodes a dual lipid and protein phosphatase that dephosphorylates the lipid phosphatidylinositol-3,4,5-trisphosphate (PIP3), in turn negatively regulating the oncogenic PI3K-AKT pathway, a key proto-oncogenic player in cancer development and progression. Because of importance of PTEN in tumorigenesis, a large number of sophisticated genetically engineered mouse models (GEMMs) has been designed to elucidate the underlying mechanisms by which the "PTEN pathway" promotes tumorigenesis, while simultaneously providing a well-tailored system for the identification of novel therapies and offering platforms for new drug discoveries. This review summarizes the major cancer mouse models through which the PTEN pathway has been genetically deconstructed, and outlines the rapid development of GEMMs toward more detailed functional and tissue-specific analysis.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Fosfatidilinositol 3-Quinasas
/
Modelos Animales de Enfermedad
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Fosfohidrolasa PTEN
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Proteínas Proto-Oncogénicas c-akt
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Neoplasias
Límite:
Animals
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Humans
Idioma:
En
Revista:
Cold Spring Harb Perspect Med
Año:
2020
Tipo del documento:
Article
País de afiliación:
Estados Unidos