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PTEN in Immunity

2022
The tumor suppressor PTEN (Phosphatase and Tensin homolog deleted on Chromosome 10) executes critical biological functions that limit cellular growth and proliferation. PTEN inhibits activation of the proto-oncogenic PI3K pathway and is required during embryogenesis and to suppress tumor formation and cancer progression throughout life.
Antonella, Papa, Pier Paolo, Pandolfi
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PTEN and Melanomagenesis

Future Oncology, 2012
The PI3K-PTEN-AKT signaling pathway is involved in various cellular activities, including proliferation, migration, cell growth, cell survival and differentiation during adult homeostasis as well as in tumorigenesis. It has been suggested that the constitutive activation of PI3K/AKT signaling with concurrent loss of function of the tumor suppressor ...
Alejandro, Conde-Perez, Lionel, Larue
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PTEN and Cancer

2003
Genetic evidence strongly suggested that a tumor suppressor was located on chromosome 10. During the development of glioblastoma, one copy of chromosome 10 was typically lost (1). Cytogenetic and molecular analysis revealed partial or complete loss of chromosome 10 in bladder, endometrial, and prostate cancer (2,3).
Ramon, Parsons, Laura, Simpson
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PTEN as a target in melanoma

Journal of Clinical Pathology, 2022
PTEN is a well-known tumour suppressor protein that is frequently found to be mutated, inactivated or deleted in a wide range of different cancers. Its tumour suppressive properties result predominantly from its inhibitory effects on the PI3K-AKT signalling pathway.
Furkan Akif Ince   +2 more
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Inhibiting PTEN

Biochemical Society Transactions, 2007
PTEN (phosphatase and tensin homologue deleted on chromosome 10) is well known as a tumour suppressor. In dephosphorylating the 3-position of the inositol ring of phosphoinositides such as PtdIns(3,4,5)P3, PTEN's lipid phosphatase activity is an important counteracting mechanism in PI3K (phosphoinositide 3-kinase) signalling. This is essential for cell
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GRPling with PTEN

Blood, 2012
Regulation of the Pten tumor suppressor is complex and mediated by varied mechanisms. In this issue of Blood , Wey and colleagues show in a biallelic conditional knockout mouse model of GRP78 and PTEN that heterozygous loss of Grp78 suppresses leukemogenesis mediated by Pten .[1][1] These ...
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