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1. James MF, Han S, Polizzano C, Plotkin SR, Manning BD, Stemmer-Rachamimov AO, Gusella JF, Ramesh V: NF2/merlin is a novel negative regulator of mTOR complex 1, and activation of mTORC1 is associated with meningioma and schwannoma growth. Mol Cell Biol; 2009 Aug;29(15):4250-61
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  • [Title] NF2/merlin is a novel negative regulator of mTOR complex 1, and activation of mTORC1 is associated with meningioma and schwannoma growth.
  • Conversely, the exogenous expression of wild-type merlin isoforms, but not a patient-derived L64P mutant, suppresses mTORC1 signaling.

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  • (PMID = 19451225.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P30 NS045776; United States / NINDS NIH HHS / NS / NS 045776; United States / NIMH NIH HHS / MH / R21 MH079213; United States / NIMH NIH HHS / MH / MH 079213; United States / NINDS NIH HHS / NS / P01 NS024279; United States / NCI NIH HHS / CA / R01 CA122617-04; United States / NINDS NIH HHS / NS / NS 024279; United States / NCI NIH HHS / CA / CA122617-04; United States / NCI NIH HHS / CA / R01 CA122617
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Multiprotein Complexes; 0 / Neurofibromin 2; 0 / Proteins; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / mechanistic target of rapamycin complex 1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2715803
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2. Alderson NL, Hama H: Fatty acid 2-hydroxylase regulates cAMP-induced cell cycle exit in D6P2T schwannoma cells. J Lipid Res; 2009 Jun;50(6):1203-8
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  • [Title] Fatty acid 2-hydroxylase regulates cAMP-induced cell cycle exit in D6P2T schwannoma cells.
  • Sphingolipids are ubiquitous components of eukaryotic cells that regulate various cellular functions.
  • In many cell types, a fraction of sphingolipids contain 2-hydroxy fatty acids, produced by fatty acid 2-hydroxylase (FA2H), as the N-acyl chain of ceramide [hydroxyl fatty acid (hFA)-sphingolipids].
  • Treatment of D6P2T Schwannoma cells with dibutyryl-cAMP (db-cAMP) induced exit from the cell cycle with concomitant upregulation of FA2H.

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  • (PMID = 19171550.001).
  • [ISSN] 0022-2275
  • [Journal-full-title] Journal of lipid research
  • [ISO-abbreviation] J. Lipid Res.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS-060807; United States / NCRR NIH HHS / RR / RR-17677
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ceramides; 0 / Fatty Acids; 0 / RNA, Small Interfering; 0 / Sphingolipids; 63X7MBT2LQ / Bucladesine; EC 1.- / Mixed Function Oxygenases; EC 1.- / fatty acid alpha-hydroxylase
  • [Other-IDs] NLM/ PMC2681402
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3. Gering KM, Marx JA, Lennartz K, Fischer C, Rajewsky MF, Kindler-Röhrborn A: The interaction mode of premalignant Schwann and immune effector cells during chemically induced carcinogenesis in the rat peripheral nervous system is strongly influenced by genetic background. Cancer Res; 2006 May 1;66(9):4708-14
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  • A point mutation of the neu/erbB-2 gene diagnostic of N-ethyl-N-nitrosourea-induced rat schwannomas is an early marker of Schwann precursor cells at high risk of subsequent malignant transformation.
  • Neu-mutant cells initially arise at a similar frequency in sensitive and resistant animals.
  • However, these cells disappear from the trigeminal nerves of resistant rats while giving rise to highly malignant schwannomas in susceptible animals.
  • The involvement of a cellular immune response was investigated in trigeminal nerves of both strains at different times after neonatal carcinogen exposure.
  • However, there were no gross differences in immune cell counts between tumor-susceptible and tumor-resistant rats, except for a moderate increase of ED2(+) macrophages in N-ethyl-N-nitrosourea-treated BDIX rats only.
  • Differential interactions of immune effector cells with premalignant Schwann cells may thus be involved in genetically determined tumor susceptibility or resistance, which could include functional differences of immune effector cells and/or a differential capability of premalignant Schwann cells to escape or counteract the cellular immune response.
  • [MeSH-major] Cell Communication / genetics. Cell Transformation, Neoplastic / genetics. Cranial Nerve Neoplasms / genetics. Leukocytes / pathology. Neurilemmoma / genetics. Precancerous Conditions / genetics. Schwann Cells / pathology
  • [MeSH-minor] Animals. Antibodies / immunology. Antigens, CD18 / immunology. Ethylnitrosourea. Immunohistochemistry. Macrophages / immunology. Macrophages / pathology. Rats. Rats, Inbred Strains. T-Lymphocytes, Cytotoxic / immunology. T-Lymphocytes, Cytotoxic / pathology. Trigeminal Nerve / drug effects. Trigeminal Nerve / pathology


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4. DeClue JE, Heffelfinger S, Benvenuto G, Ling B, Li S, Rui W, Vass WC, Viskochil D, Ratner N: Epidermal growth factor receptor expression in neurofibromatosis type 1-related tumors and NF1 animal models. J Clin Invest; 2000 May;105(9):1233-41
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  • [Title] Epidermal growth factor receptor expression in neurofibromatosis type 1-related tumors and NF1 animal models.
  • We have found that EGF-R expression is associated with the development of the Schwann cell-derived tumors characteristic of neurofibromatosis type 1 (NF1) and in animal models of this disease.
  • Consistent with this hypothesis, growth of NF1 MPNST lines and the transformed NF1(-/-) mouse embryo Schwann cells was greatly stimulated by EGF in vitro and could be blocked by agents that antagonize EGF-R function.


5. Watanabe T, Nagase K, Chosa M, Tobinai K: Schwann cell autophagy induced by SAHA, 17-AAG, or clonazepam can reduce bortezomib-induced peripheral neuropathy. Br J Cancer; 2010 Nov 9;103(10):1580-7
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  • A tractable system to evaluate combination drugs for use with bortezomib is essential to enable continuing clinical benefit from this drug.
  • METHODS: Rat schwannoma cells were pretreated with vincristine (VCR), histone deacetylase inhibitors, anticonvulsants, or a heat-shock protein 90 (HSP90) inhibitor.
  • To then monitor aggresome formation as a result of proteasome inhibition and the activation of chaperone-mediated autophagy (CMA), we performed double-labelling immunofluorescent analyses of a cellular aggregation-prone protein marker.
  • RESULTS: Aggresome formation was interrupted by VCR, whereas combination treatments with bortezomib involving suberoylanilide hydroxamic acid, 17-allylamino-17-demethoxy-geldanamycin, or clonazepam appear to facilitate the disposal of unfolded proteins via CMA, inducing HSP70 and lysosome-associated membrane protein type 2A (LAMP-2A).
  • CONCLUSIONS: This schwannoma model can be used to test BiPN-reducing drugs.
  • The present data suggest that aggresome formation in Schwann cells is a possible mechanism of BiPN, and drugs that induce HSP70 or LAMP-2A have the potential to alleviate this complication.
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Bortezomib. Cell Division / drug effects. Cell Line, Tumor. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Multiple Myeloma / drug therapy. Multiple Myeloma / pathology. Neurilemmoma. Protein Folding. Proteostasis Deficiencies / pathology. Pyrazines / therapeutic use. Rats. Schwann Cells / cytology. Schwann Cells / pathology

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  • (PMID = 20959823.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoquinones; 0 / Boronic Acids; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Pyrazines; 4GY0AVT3L4 / tanespimycin; 5PE9FDE8GB / Clonazepam; 69G8BD63PP / Bortezomib
  • [Other-IDs] NLM/ PMC2990589
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6. Yi C, Wilker EW, Yaffe MB, Stemmer-Rachamimov A, Kissil JL: Validation of the p21-activated kinases as targets for inhibition in neurofibromatosis type 2. Cancer Res; 2008 Oct 1;68(19):7932-7
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  • [Title] Validation of the p21-activated kinases as targets for inhibition in neurofibromatosis type 2.
  • Neurofibromatosis type 2 (NF2) is a dominantly inherited cancer disorder caused by mutations at the NF2 gene locus.
  • Merlin, the protein product of the NF2 gene, has been shown to negatively regulate Rac1 signaling by inhibiting its downstream effector kinases, the p21-activated kinases (Pak).
  • First, analysis of primary schwannoma samples derived from NF2 patients showed that in a significant fraction of the tumors, the activity of Pak1 was highly elevated.
  • Finally, while attempting to silence Pak1 in rat schwannoma cells, we found that these cells were unable to tolerate long-term Pak1 inhibition and rapidly moved to restore Pak1 levels by shutting down Pak1 shRNA expression through a methylation-dependent mechanism.

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  • (PMID = 18829550.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA124495; United States / NCI NIH HHS / CA / F32 CA123752-01; United States / NCI NIH HHS / CA / F32 CA123752-03; United States / NINDS NIH HHS / NS / NS024279-19; United States / NCI NIH HHS / CA / CA101502-02; United States / NINDS NIH HHS / NS / P01 NS024279-19; United States / NCI NIH HHS / CA / CA123752-01; United States / NCI NIH HHS / CA / CA123752-02; United States / NCI NIH HHS / CA / F32 CA101502-02; United States / NCI NIH HHS / CA / CA123752-03; United States / NCI NIH HHS / CA / F32 CA101502; United States / NINDS NIH HHS / NS / P01 NS024279; United States / NCI NIH HHS / CA / F32 CA123752-02; United States / NCI NIH HHS / CA / F32 CA123752
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; EC 2.7.11.1 / p21-Activated Kinases
  • [Other-IDs] NLM/ NIHMS112457; NLM/ PMC2707059
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7. Prkacin I, Martinac M, Sabljar-Matovinović M, Skegro D, Mazalin J: Pelvic neurilemmoma. Acta Med Croatica; 2001;55(2):97-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pelvic neurilemmoma.
  • A case of a 37-year-old man admitted to our Department of Internal Medicine for medical evaluation of hypertension is reported.
  • Histopathologic analysis of the tumor, 11 x 8 x 8 cm in size, composed of cellular and mixoid areas with traces of collagenous connective tissue, necrosis, and tiny calcifications with scattered palisading nuclei and Verocay bodies, pointed to the diagnosis of a benign tumor, i.e. neurilemmoma.
  • To our knowledge, pelvic localization of neurilemmoma, particularly a large one, is rare.
  • [MeSH-major] Neurilemmoma. Pelvic Neoplasms. Retroperitoneal Neoplasms

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  • (PMID = 11505636.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
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8. Yamate J, Yasui H, Benn SJ, Tsukamoto Y, Kuwamura M, Kumagai D, Sakuma S, LaMarre J: Characterization of newly established tumor lines from a spontaneous malignant schwannoma in F344 rats: nerve growth factor production, growth inhibition by transforming growth factor-beta1, and macrophage-like phenotype expression. Acta Neuropathol; 2003 Sep;106(3):221-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of newly established tumor lines from a spontaneous malignant schwannoma in F344 rats: nerve growth factor production, growth inhibition by transforming growth factor-beta1, and macrophage-like phenotype expression.
  • Transplantable tumor (KE) and clone cell (KE-F11) lines were established from a spontaneous malignant schwannoma found in an aged F344 rat.
  • Likely, TGF-beta1 is a factor capable of inhibiting cellular growth of Schwann cells. mRNA expression of the low-density lipoprotein receptor-related protein (LRP) was seen in KE-F11 cells by Northern blot analysis, and the level was decreased by lipopolysaccharide (LPS) treatment.
  • KE-F11 cells seeded on laminin-coated dishes exhibited more extended cytoplasmic projections than on collagen type I-coated dishes.
  • The present study provides evidence that biological properties of malignant schwannoma-derived cells might be affected by exogenous factors such as TGF-beta1, LPS and laminin.
  • [MeSH-major] Macrophages / ultrastructure. Nerve Growth Factor / metabolism. Neurilemmoma / metabolism. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Actins / metabolism. Animals. Blotting, Northern. Cell Count. Cell Line, Transformed. Desmin / metabolism. Dose-Response Relationship, Drug. Genes, jun / physiology. Genes, myc / physiology. Glial Fibrillary Acidic Protein / metabolism. In Vitro Techniques. Keratins / metabolism. Lipopolysaccharides / pharmacology. Male. Microscopy, Electron. Myelin Basic Protein / metabolism. PC12 Cells. Phenotype. Phosphopyruvate Hydratase / metabolism. RNA, Messenger / biosynthesis. Rats. Rats, Inbred F344. Reverse Transcriptase Polymerase Chain Reaction / methods. S100 Proteins / metabolism. Staining and Labeling. Time Factors. Transforming Growth Factor beta1. Vimentin / metabolism

  • Cellosaurus - a cell line knowledge resource. culture/stock collections - Cellosaurus - a cell line knowledge resource .
  • Cellosaurus - a cell line knowledge resource. culture/stock collections - Cellosaurus - a cell line knowledge resource .
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  • (PMID = 12811582.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Actins; 0 / Desmin; 0 / Glial Fibrillary Acidic Protein; 0 / Lipopolysaccharides; 0 / Myelin Basic Protein; 0 / RNA, Messenger; 0 / S100 Proteins; 0 / Tgfb1 protein, rat; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Vimentin; 68238-35-7 / Keratins; 9061-61-4 / Nerve Growth Factor; EC 4.2.1.11 / Phosphopyruvate Hydratase
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9. Kindler-Röhrborn A, Kind AB, Koelsch BU, Fischer C, Rajewsky MF: Suppression of ethylnitrosourea-induced schwannoma development involves elimination of neu/erbB-2 mutant premalignant cells in the resistant BDIV rat strain. Cancer Res; 2000 Sep 1;60(17):4756-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppression of ethylnitrosourea-induced schwannoma development involves elimination of neu/erbB-2 mutant premalignant cells in the resistant BDIV rat strain.
  • In BDIX rats, a point mutation at nucleotide 2012 in the transmembrane region of the neu/erbB-2 gene has proved to be a very early marker of initiated Schwann precursor cells with an elevated risk of malignant transformation, and is diagnostic of the resulting schwannomas.
  • To gain insight into the cellular and molecular mechanisms responsible for the resistance of the BDIV strain, comparative quantitative neu mutation analyses combined with histomorphological studies were performed on the trigeminal nerves of EtNU-treated BDIV and BDIX rats as well as on their (BDIX x BDIV) F1 progeny.
  • It was found that neu-mutant Schwann cells are initially present at comparable frequency in the trigeminal nerves of both resistant and sensitive animals.
  • Contrasting with the progressive multiplication of mutant Schwann cells in BDIX trigeminal nerves, however, the numbers of mutant cells began to decrease during the intermediary phase of the carcinogenic process in BDIV animals, and premalignant neu-mutant cells were no longer detectable by the time BDIX rats developed full-blown trigeminal schwannomas.
  • [MeSH-major] Cranial Nerve Neoplasms / genetics. Genes, erbB-2 / physiology. Genetic Predisposition to Disease / genetics. Neurilemmoma / genetics. Precancerous Conditions / genetics
  • [MeSH-minor] Alleles. Animals. Carcinogens. Crosses, Genetic. Ethylnitrosourea. Female. Male. Point Mutation / physiology. Rats. Rats, Inbred Strains. Trigeminal Nerve / drug effects. Trigeminal Nerve / pathology. Trigeminal Nerve / physiology






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