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lipoma/phosphatase
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Resveratrol Potentiates Growth Inhibitory Effects of Rapamycin in PTEN-deficient Lipoma Cells by Suppressing p70S6 Kinase Activity.
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Patients with phosphatase and tensin homolog (PTEN) hamartoma tumor syndrome and germline mutations in PTEN frequently develop lipomatosis, for which there is no standard treatment. Rapamycin was shown to reduce the growth of lipoma cells with heterozygous PTEN deficiency in vitro, but concomitantly
Do Mesenchymal Stem Cells Derived From Atypical Lipomatous Tumors Have Greater Differentiation Potency Than Cells From Normal Adipose Tissues?
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BACKGROUND
The p53 protein in mesenchymal stem cells (MSCs) regulates differentiation to osteogenic or adipogenic lineage. Because p53 function is depressed in most malignancies, if MSCs in malignancy also have p53 hypofunction, differentiation therapy to osteogenic or adipogenic lineage may be an
ZRP-1, a zyxin-related protein, interacts with the second PDZ domain of the cytosolic protein tyrosine phosphatase hPTP1E.
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Protein-protein interactions play an important role in the specificity of cellular signaling cascades. By using the yeast two-hybrid system, a specific interaction was identified between the second PDZ domain of the cytosolic protein tyrosine phosphatase hPTP1E and a novel protein, which was termed
Identification of PPAP2B as a novel recurrent translocation partner gene of HMGA2 in lipomas.
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Most lipomas are characterized by translocations involving the HMGA2 gene in 12q14.3. These rearrangements lead to the fusion of HMGA2 with an ectopic sequence from the translocation chromosome partner. Only five fusion partners of HMGA2 have been identified in lipomas so far. The identification of
Enhanced expression of catalytic subunits of protein phosphatase type 1 and high S-phase fraction in liposarcoma.
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The expression of the three catalytic subunits of protein phosphatase (PP) type 1 and 2A, PP1 alpha, PP1 gamma 1, and PP2AC, was examined in 8 cases of lipoma as a benign tumor and 4 cases of liposarcoma as a malignant tumor using immunohistochemical analysis. Both types of of tumor cells stained
Investigation of protein-tyrosine phosphatase 1B function by quantitative proteomics.
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Because of their antagonistic catalytic functions, protein-tyrosine phosphatases (PTPs) and protein-tyrosine kinases act together to control phosphotyrosine-mediated signaling processes in mammalian cells. However, unlike for protein-tyrosine kinases, little is known about the cellular substrate
Role of protein phosphatase in malignant osteogenic and soft tissue tumors.
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The expression of the three catalytic subunits of protein phosphatase (PP) type 1 and 2A, PP1 alpha, PP1 gamma 1, and PP2AC, was examined in osteogenic tumors and soft tissue tumors by immunohistochemical analysis. The percentage of cells stained positively with antiserum against PP1 catalytic
Investigation of stemness and multipotency of equine adipose-derived mesenchymal stem cells (ASCs) from different fat sources in comparison with lipoma.
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Simvastatin induces apoptosis in PTEN‑haploinsufficient lipoma cells.
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Adipose tissue tumors (lipomas) frequently develop in patients with heterozygous germ line phosphatase and tensin homolog (PTEN) mutations. simvastatin has been demonstrated to exhibit antitumor effects, and so the aim of the present study was to assess the effects of simvastatin on the growth of
PP2A binds to the LIM domains of lipoma-preferred partner through its PR130/B″ subunit to regulate cell adhesion and migration.
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Here, we identify the LIM protein lipoma-preferred partner (LPP) as a binding partner of a specific protein phosphatase 2A (PP2A) heterotrimer that is characterised by the regulatory PR130/B″α1 subunit (encoded by PPP2R3A). The PR130 subunit interacts with the LIM domains of LPP through a conserved
Intermediate uveitis in a child with phosphatase and tensin homolog gene mutation and Bannayan-Riley-Ruvalcaba syndrome.
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Bannayan-Riley-Ruvalcaba syndrome (BRRS) is a congenital disorder characterised by macrocephaly, multiple hamartomas, lipomas, and pigmented macules of the glans penis. Intermediate uveitis is characterised by chronic inflammatory cells aggregates on the pars plana (snowbanks) and within the
Thyroid involvement in two patients with Bannayan-Riley-Ruvalcaba syndrome.
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Bannayan-Riley-Ruvalcaba syndrome (BRRs) is an overgrowth disorder characterized by macrocephaly, pigmented maculae of the glans penis, and benign mesodermal hamartomas (primarily subcutaneous and visceral lipomas, multiple hemangiomas, and intestinal polyps). Dysmorphic features as well as delayed
Bannayan-Riley-Ruvalcaba Syndrome in a Patient with a PTEN Mutation Identified by Chromosomal Microarray Analysis: A Case Report.
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Bannayan-Riley-Ruvalcaba syndrome (BRRS) is one of the phosphatase and tensin homolog hamartoma tumor syndrome with a PTEN gene mutation. It is a rare dominant autosomal disorder characterized by cutaneous lipomas, macrocephaly, intestinal polyps, and developmental delay. Diagnosing this syndrome is
Analysis of PTEN gene mutations in a Turkish patient with Cowden syndrome.
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Cowden syndrome (CS), an autosomal dominant disorder, is associated with germline mutations of the PTEN (phosphatase, tensin homolog, deleted on chromosome TEN) gene. PTEN mutations were linked to several human neoplasms. Clinical diagnosis has been based on Consortium criteria, but detection of
Novel PTEN germline mutation in a family with mild phenotype: difficulties in genetic counseling.
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PTEN gene (phosphatase and tensin homolog deleted on chromosome ten, MIM 601628) is a tumor suppressor gene implicated in PTEN hamartoma tumor syndromes (PHTS) including Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome and Proteus-like syndrome. PTEN mutations have been more recently reported in
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