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1. Pandhi D, Singal A, Aggarwal S: Adult onset, hypopigmented solitary mastocytoma: report of two cases. Indian J Dermatol Venereol Leprol; 2008 Jan-Feb;74(1):41-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult onset, hypopigmented solitary mastocytoma: report of two cases.
  • Solitary mastocytoma is known to occur predominantly in children below 2 years of age and onset in adulthood is rare.
  • Lesions are hyperpigmented in the majority of cases owing to the stimulation of melanin synthesis by mast cell growth factor.
  • We hereby report two patients with adult onset solitary mastocytoma presenting as hypopigmented plaque.
  • Histopathology revealed a dense toluidine blue-positive infiltrate of mast cells in the upper dermis in both cases.
  • [MeSH-major] Hypopigmentation / pathology. Mastocytoma, Skin / pathology
  • [MeSH-minor] Adult. Age of Onset. Biopsy. Dermis / pathology. Eosinophils / pathology. Humans. Male. Mast Cells / pathology. Neck

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  • (PMID = 18187823.001).
  • [ISSN] 0973-3922
  • [Journal-full-title] Indian journal of dermatology, venereology and leprology
  • [ISO-abbreviation] Indian J Dermatol Venereol Leprol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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2. Takahashi T, Ohashi E, Nakagawa T, Mochizuki M, Nishimura R, Sasaki N: Role of beta1 integrins in adhesion of canine mastocytoma cells to extracellular matrix proteins. J Vet Med Sci; 2007 May;69(5):495-9
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  • [Title] Role of beta1 integrins in adhesion of canine mastocytoma cells to extracellular matrix proteins.
  • The interactions of tumor cells with the extracellular matrix (ECM) are a crucial step in invasion and metastasis.
  • In this study, mastocytoma (mast cell tumor: MCT) cell-ECM interaction was investigated using 3 canine MCT cell lines: CM-MC (originating from cutaneous MCT), VI-MC (originating from intestinal MCT), and CoMS (originating from oral MCT).
  • In adhesion studies, CoMS weakly but spontaneously adhered to fibronectin (FN), which was enhanced by phorbol ester (TPA), while CM-MC and VI-MC required cell activation by TPA to adhere to FN.
  • Anti-beta1 and alpha5 integrin antibodies strongly inhibited cell adhesion to FN in CM-MC and CoMS and moderately inhibited cell adhesion in VI-MC.
  • Anti-beta1 integrin antibodies strongly inhibited cell adhesion to LN, but all anti-alpha integrin antibodies failed to inhibit cell adhesion to LN.

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  • (PMID = 17551222.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Extracellular Matrix Proteins; 0 / Integrin beta Chains
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3. Yee SB, Baek SJ, Park HT, Jeong SH, Jeong JH, Kim TH, Kim JM, Jeong BK, Park BS, Kwon TK, Yoon I, Yoo YH: zVAD-fmk, unlike BocD-fmk, does not inhibit caspase-6 acting on 14-3-3/Bad pathway in apoptosis of p815 mastocytoma cells. Exp Mol Med; 2006 Dec 31;38(6):634-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] zVAD-fmk, unlike BocD-fmk, does not inhibit caspase-6 acting on 14-3-3/Bad pathway in apoptosis of p815 mastocytoma cells.
  • In a preliminary study, we found that benzyloxycarbonyl-Val-Ala-Asp(OMe)-fluoromethylketone (zVAD- fmk), unlike Boc-aspartyl(OMe)-fluoromethylketone (BocD-fmk), at usual dosage could not prevent genistein-induced apoptosis of p815 mastocytoma cells.
  • [MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Animals. Caspase Inhibitors. Cell Line, Tumor. Genistein / pharmacology. Mastocytoma. Mice. Mitochondria / drug effects

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  • (PMID = 17202839.001).
  • [ISSN] 1226-3613
  • [Journal-full-title] Experimental & molecular medicine
  • [ISO-abbreviation] Exp. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / 14-3-3 Proteins; 0 / Amino Acid Chloromethyl Ketones; 0 / Benzyl Compounds; 0 / Boc-D-FMK; 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / Hydrocarbons, Fluorinated; 0 / bcl-Associated Death Protein; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; DH2M523P0H / Genistein; EC 3.4.22.- / Caspase 6
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4. Furuta K, Nakayama K, Sugimoto Y, Ichikawa A, Tanaka S: Activation of histidine decarboxylase through post-translational cleavage by caspase-9 in a mouse mastocytoma P-815. J Biol Chem; 2007 May 4;282(18):13438-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activation of histidine decarboxylase through post-translational cleavage by caspase-9 in a mouse mastocytoma P-815.
  • We investigated the processing of HDC in a mouse mastocytoma, P-815, using a lentiviral expression system.
  • Although treatment with butyrate and TPEN drastically augmented the protease activity of caspase-3, and -9, no apoptotic cell death was observed.
  • [MeSH-major] Apoptosis. Caspase 9 / metabolism. Histidine Decarboxylase / metabolism. Mastocytoma / enzymology. Neoplasm Proteins / metabolism. Protein Processing, Post-Translational
  • [MeSH-minor] Animals. Aspartic Acid / genetics. Aspartic Acid / metabolism. Caspase 3 / genetics. Caspase 3 / metabolism. Cell Line, Tumor. Chelating Agents / pharmacology. Ethylenediamines / pharmacology. Histamine / biosynthesis. Humans. Lentivirus. Mice. Protease Inhibitors / pharmacology. Protein Precursors / genetics. Protein Precursors / metabolism. Zinc / metabolism

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  • (PMID = 17360717.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chelating Agents; 0 / Ethylenediamines; 0 / Neoplasm Proteins; 0 / Protease Inhibitors; 0 / Protein Precursors; 16858-02-9 / N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine; 30KYC7MIAI / Aspartic Acid; 820484N8I3 / Histamine; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9; EC 4.1.1.22 / Histidine Decarboxylase; J41CSQ7QDS / Zinc
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5. Maxová H, Bacáková L, Eckhardt A, Miksík I, Lisá V, Novotná J, Herget J: Growth of vascular smooth muscle cells on collagen I exposed to RBL-2H3 mastocytoma cells. Cell Physiol Biochem; 2010;25(6):615-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth of vascular smooth muscle cells on collagen I exposed to RBL-2H3 mastocytoma cells.
  • The aim of this "in vitro" study was to verify that mast cells (RBL-2H3) as a potent source of a variety of biomolecules which can affect vessel wall remodeling are capable of splitting collagen and then facilitating the growth of vascular smooth muscle cells (VSMC).
  • The VSMC proliferated with the shortest doubling time and reached the highest cell population density on the collagen pre-modified with hypoxic RBL-2H3 cells.
  • Mast cells exposed to hypoxia are more capable to split collagen and facilitate the growth of VSMC.
  • [MeSH-major] Cell Proliferation. Collagen Type I / metabolism. Mast Cells / metabolism. Muscle, Smooth, Vascular / cytology
  • [MeSH-minor] Amino Acid Sequence. Animals. Aorta / cytology. Cell Adhesion. Cell Hypoxia. Cell Line, Tumor. Cells, Cultured. Male. Mastocytoma / metabolism. Molecular Sequence Data. Rats. Rats, Wistar

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20511706.001).
  • [ISSN] 1421-9778
  • [Journal-full-title] Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
  • [ISO-abbreviation] Cell. Physiol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Collagen Type I
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6. Alsharqi A, Parslew R, Shukla R: A 3-month-old with a blistering plaque. Dermatol Online J; 2010;16(9):10

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We present a case of a 3-month-old child with a solitary mastocytoma who was initially diagnosed with recurrent bullous impetigo.
  • Solitary mastocytoma can present as a blister.
  • Although bullous impetigo is a common diagnosis in children and it would be tempting to make that diagnosis in the presence of a positive skin swab culture, clinicians always have to be mindful of secondary impetiginization of another primary skin disease process.
  • [MeSH-major] Mastocytoma, Skin / diagnosis

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  • (PMID = 20875331.001).
  • [ISSN] 1087-2108
  • [Journal-full-title] Dermatology online journal
  • [ISO-abbreviation] Dermatol. Online J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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7. Krop M, van Veghel R, Garrelds IM, de Bruin RJ, van Gool JM, van den Meiracker AH, Thio M, van Daele PL, Danser AH: Cardiac Renin levels are not influenced by the amount of resident mast cells. Hypertension; 2009 Aug;54(2):315-21

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cardiac Renin levels are not influenced by the amount of resident mast cells.
  • To investigate whether mast cells release renin in the heart, we studied renin and prorenin synthesis by such cells, using the human mast cell lines human mastocytoma 1 and LAD2, as well as fresh mast cells from mastocytosis patients.
  • We also quantified the contribution of mast cells to cardiac renin levels in control and infarcted rat hearts.
  • Human mastocytoma 1 cells contained and released angiotensin I-generating activity, and the inhibition of this activity by the renin inhibitor aliskiren was comparable to that of recombinant human renin.
  • Angiotensin I-generating activity was undetectable in LAD2 cells and fresh mast cells.
  • Results in infarcted hearts were identical, despite the increased mast cell number in such hearts.
  • In conclusion, human mastocytoma 1 cells release renin and prorenin, and the regulation of this release resembles that of renal renin.
  • However, this is not a uniform property of all mast cells.
  • Mast cells appear an unlikely source of renin in the heart, both under normal and pathophysiological conditions.
  • [MeSH-major] Mast Cells / metabolism. Myocardium / metabolism. Renin / metabolism. Renin-Angiotensin System / physiology
  • [MeSH-minor] Adult. Aged. Analysis of Variance. Angiotensin I / pharmacology. Animals. Cells, Cultured. Disease Models, Animal. Female. Humans. Male. Myocytes, Cardiac / metabolism. Probability. Random Allocation. Rats. Rats, Sprague-Dawley

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  • (PMID = 19564544.001).
  • [ISSN] 1524-4563
  • [Journal-full-title] Hypertension (Dallas, Tex. : 1979)
  • [ISO-abbreviation] Hypertension
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9041-90-1 / Angiotensin I; EC 3.4.23.15 / Renin
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8. Sasai K, Katoh M, Fujita D, Yamashita M, Constantinoiu CC, Matsubayashi M, Tani H, Baba E: Monoclonal antibodies for the diagnosis of canine mastocytoma. Hybridoma (Larchmt); 2007 Jun;26(3):162-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monoclonal antibodies for the diagnosis of canine mastocytoma.
  • Mastocytomas are the most common malignant neoplasm in the dog; they are more aggressive than the mast cell tumors of other species.
  • Therefore, it is imperative to develop a highly sensitive and specific immunoassay for clinical diagnosis of canine mastocytoma.
  • The production and characterization of new mouse monoclonal antibodies (MAb 9-3 and MAb 80) directed against canine mastocytoma are reported here.
  • By immunohistochemistry using fresh frozen tissue of tissue impression smears, we observed that the antigen recognized by MAb 9-3 is expressed exclusively on the surface and cytoplasmic granules of canine mastocytoma but not on the mast cells in normal canine skin.
  • MAb 80 did not compete for binding to mast cells in normal canine skin.
  • Western blot assays performed with canine mastocytoma indicated that MAb 9-3 recognized the 74 kDa band, and MAb 80 recognized the 167 and 248 kDa bands.
  • We studied the immunostaining pattern of impression smears with MAb 9-3 from 36 benign and malignant canine masses, including eight samples of mastocytoma that were positive and other tumor samples that were negative by MAb 9-3.
  • This report for the first time precisely characterizes a monoclonal antibody specific for canine mastocytoma, facilitating clinical and molecular investigation of canine mastocytoma.
  • [MeSH-major] Antibodies, Monoclonal. Dog Diseases / diagnosis. Mast-Cell Sarcoma / veterinary
  • [MeSH-minor] Animals. Antigens, Neoplasm. Cross Reactions. Dogs. Female. Hybridomas / immunology. Male. Mast Cells / immunology. Mastocytoma / diagnosis. Mastocytoma / immunology. Mastocytoma / veterinary. Mice. Mice, Inbred BALB C. Skin / immunology. Skin Neoplasms / diagnosis. Skin Neoplasms / immunology. Skin Neoplasms / veterinary

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  • (PMID = 17600498.001).
  • [ISSN] 1554-0014
  • [Journal-full-title] Hybridoma (2005)
  • [ISO-abbreviation] Hybridoma (Larchmt)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm
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9. Mederle O, Mederle N, Bocan EV, Ceauşu R, Raica M: VEGF expression in dog mastocytoma. Rev Med Chir Soc Med Nat Iasi; 2010 Jan-Mar;114(1):185-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] VEGF expression in dog mastocytoma.
  • The biologic behavior of mastocytomas is highly variable; some tumors have a benign behavior, whereas others exhibit aggressive growth and metastasis.
  • MATERIAL AND METHOD: In the present study, we have investigated expression of VEGF in cutaneous tumor from a dog and combined immunohistochemical expression of VEGF with mast cell tryptase, CD117 and vimentin.
  • RESULTS: Tumor cells were positive for VEGF, and inflammatory cells were negative.
  • VEGF expression was found in tumor cells as a heterogeneous positive reaction, with cytoplasmic pattern and moderate to strong in intensity.
  • Arrangement of tumor cells was in clusters, in deepest part, close to the proliferation front.
  • The dog died 5 month from the diagnosis, and our observation suggest that VEGF secretion by tumor cells correlates with unfavorable prognosis.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Dog Diseases / metabolism. Mastocytoma / veterinary. Skin Neoplasms / veterinary. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 20509299.001).
  • [ISSN] 0048-7848
  • [Journal-full-title] Revista medico-chirurgicală̆ a Societă̆ţ̜ii de Medici ş̧i Naturaliş̧ti din Iaş̧i
  • [ISO-abbreviation] Rev Med Chir Soc Med Nat Iasi
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor A; 0 / Vimentin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.21.59 / Tryptases
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10. Turin L, Acocella F, Stefanello D, Oseliero A, Fondrini D, Brizzola S, Riva F: Expression of c-kit proto-oncogene in canine mastocytoma: a kinetic study using real-time polymerase chain reaction. J Vet Diagn Invest; 2006 Jul;18(4):343-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of c-kit proto-oncogene in canine mastocytoma: a kinetic study using real-time polymerase chain reaction.
  • KIT receptor, the c-kit gene product, is thought to play a major role in canine mastocytoma, one of the most common neoplastic diseases in dogs.
  • In the present study, the expression of c-kit proto-oncogene in blood and in tumor biopsies from 41 dogs with histologically confirmed mastocytoma at different grades of cellular differentiation and 5 negative control dogs was investigated using real-time (quantitative) reverse transcription-polymerase chain reaction (RRT-PCR).
  • Transcript mRNAs extracted from blood at different time points after surgery and from tumor tissue surgically removed from each dog were used in a quantitative RRT-PCR assay targeting the extracellular coding region of the c-kit gene.
  • Levels of expression of c-kit were higher in tumor biopsies than in blood; the blood level decreased in the patients between 1 and 3 months after surgery.
  • No KIT expression was detected in blood from the 5 dogs not affected by mastocytoma (negative controls).
  • Although c-kit expression levels measured by RRT-PCR do not correlate with prognosis, they confirm that surgery remains the main treatment to reduce circulating mastocytes and that circulating mast cells can be detected even in benign highly differentiated forms of mastocytoma such as grade I.
  • [MeSH-major] Dog Diseases / genetics. Gene Expression Regulation, Neoplastic. Mastocytoma / veterinary. Polymerase Chain Reaction / veterinary. Proto-Oncogene Proteins c-kit / genetics

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  • (PMID = 16921872.001).
  • [ISSN] 1040-6387
  • [Journal-full-title] Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
  • [ISO-abbreviation] J. Vet. Diagn. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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11. Matsumoto M, Ikeda M, Takeya M, Kodama H: Plane xanthoma associated with multiple mastocytoma. Pediatr Dermatol; 2007 Sep-Oct;24(5):E66-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Plane xanthoma associated with multiple mastocytoma.
  • The brown macules showed infiltration of a large number of mast cells and a small number of scattered foam cells, whereas in the yellowish plaques, the number of foam cells was greatly increased.
  • Therefore, the yellowish plaques were considered to be plane xanthoma associated with cutaneous mastocytoma.
  • [MeSH-minor] Foam Cells / pathology. Humans. Infant. Male. Mast Cells / pathology

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  • (PMID = 17958784.001).
  • [ISSN] 1525-1470
  • [Journal-full-title] Pediatric dermatology
  • [ISO-abbreviation] Pediatr Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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12. Salces IG, Alfaro J, Sáenz DE Santamaría MC, Sanchez M: Scabies presenting as solitary mastocytoma-like eruption in an infant. Pediatr Dermatol; 2009 Jul-Aug;26(4):486-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Scabies presenting as solitary mastocytoma-like eruption in an infant.
  • We report a case in which the initial clinical finding was a solitary cutaneous nodule on the wrist of a young infant which urticated when rubbed, and was diagnosed as a solitary mastocytoma.
  • While scabies has been reported to mimick a variety of conditions including urticaria pigmentosa, to our knowledge no previous cases masquerading as solitary mastocytoma have been reported.
  • [MeSH-major] Mastocytoma, Skin / pathology. Scabies / pathology. Skin Neoplasms / pathology

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  • (PMID = 19689539.001).
  • [ISSN] 1525-1470
  • [Journal-full-title] Pediatric dermatology
  • [ISO-abbreviation] Pediatr Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insecticides; 0 / Ointments; 509F88P9SZ / Permethrin
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13. Benamar M, Melhaoui A, Zyad A, Bouabdallah I, Aziz M: Anti-cancer effect of two alkaloids: 2R and 2S-bgugaine on mastocytoma P815 and carcinoma Hep. Nat Prod Res; 2009;23(7):659-64

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  • [Title] Anti-cancer effect of two alkaloids: 2R and 2S-bgugaine on mastocytoma P815 and carcinoma Hep.
  • Tozz. (Araceae), and its isomer S-bgugaine, obtained by an asymmetric synthesis, were examined for their cytotoxic activities on two cancerous cellular lines: the murine mastocytoma cell line P815 and the human laryngeal carcinoma cell line Hep.
  • The concentrations required to induce 50% of lysis (IC(50)) for R-bgugaine and S-bgugaine alkaloids were determined, and are 10 and 5 microg mL(-1), and 5 and 100 microg mL(-1), respectively, for the mastocytoma P815 and carcinoma Hep, compared with those of Adriamycine (5 microg mL(-1) for P815 cell line and 5 microg mL(-1) for Hep cell line), taken as positive controls.
  • [MeSH-minor] Animals. Cell Death / drug effects. Cell Line, Tumor. Humans. Inhibitory Concentration 50. Mice. Molecular Structure

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  • (PMID = 19401921.001).
  • [ISSN] 1478-6427
  • [Journal-full-title] Natural product research
  • [ISO-abbreviation] Nat. Prod. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Antineoplastic Agents; 0 / Cytotoxins; 0 / Pyrrolidines; 0 / bgugaine
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14. Tuxen AJ, Orchard D: Solitary mastocytoma occurring at a site of trauma. Australas J Dermatol; 2009 May;50(2):133-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Solitary mastocytoma occurring at a site of trauma.
  • We describe a patient with a solitary mastocytoma arising at a site of trauma.
  • The patient was born with the umbilical cord wrapped around her right thigh and subsequently developed a solitary mastocytoma in the exact site and distribution of this injury.
  • The pathogenesis of mast cell proliferation in solitary mastocytoma is not completely understood.
  • Cytokines released after injury, such as stem cell factor, may stimulate the proliferation of mast cells, as well as fibroblasts and melanocytes to form a mastocytoma.
  • Mast cells in a newborn may be more sensitive to stem cell factor in the presence of cytokines released after injury due to an increased density of c-kit receptors.
  • [MeSH-major] Birth Injuries / physiopathology. Mastocytoma, Skin / diagnosis. Mastocytoma, Skin / etiology. Thigh / injuries. Wound Healing / physiology

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  • (PMID = 19397569.001).
  • [ISSN] 1440-0960
  • [Journal-full-title] The Australasian journal of dermatology
  • [ISO-abbreviation] Australas. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 826Y60901U / betamethasone-17,21-dipropionate; 9842X06Q6M / Betamethasone; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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15. Tran DT, Jokinen CH, Argenyi ZB: Histiocyte-rich pleomorphic mastocytoma: an uncommon variant mimicking juvenile xanthogranuloma and Langerhans cell histiocytosis. J Cutan Pathol; 2009 Nov;36(11):1215-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histiocyte-rich pleomorphic mastocytoma: an uncommon variant mimicking juvenile xanthogranuloma and Langerhans cell histiocytosis.
  • A biopsy demonstrated a large intradermal nodule composed of unusually large epithelioid mast cells, including a prominent subset with bi-lobed and multi-lobed nuclei.
  • By immunohistochemistry, the cells expressed CD117 (C-Kit), mast cell tryptase, CD68, and CD25, and were negative for CD163, CD1a, and S-100, confirming the diagnosis of mastocytoma.
  • However, given the unusual cytologic features, close clinical observation is warranted, as the long-term biologic potential of mastocytoma with this degree of cytologic atypia is uncertain.
  • Awareness of this unusual morphologic variant is also important as the histologic features may mimic such childhood neoplasms as juvenile xanthogranuloma and Langerhans cell histiocytosis.
  • [MeSH-major] Histiocytes / pathology. Mastocytoma / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Child. Diagnosis, Differential. Female. Histiocytosis, Langerhans-Cell / pathology. Humans. Immunohistochemistry. Neck / pathology. Xanthogranuloma, Juvenile / pathology


16. Bussmann C, Hagemann T, Hanfland J, Haidl G, Bieber T, Novak N: Flushing and increase of serum tryptase after mechanical irritation of a solitary mastocytoma. Eur J Dermatol; 2007 Jul-Aug;17(4):332-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Flushing and increase of serum tryptase after mechanical irritation of a solitary mastocytoma.
  • Solitary mastocytomas are infiltrates of mast cells in the upper corium, appearing at any side of the body as brownish-reddish plaques in the first months of life.
  • Their course is benign with a spontaneous regression in most cases.
  • We conclude that uncontrolled stroking of mastocytomas should be avoided in patients with a systemic reaction in their history, since this case demonstrates that despite its limited size, mechanical irritation of a solitary mastocytoma may induce strong systemic symptoms as witnessed by transient increase of the serum tryptase, which to our knowledge has not been described in the literature before.
  • [MeSH-major] Flushing / etiology. Mastocytoma / blood. Mastocytoma / complications. Tryptases / blood

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  • (PMID = 17540642.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] EC 3.4.21.59 / Tryptases
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17. Fulciniti F, Di Mattia D, Curcio MP, Bove P, Rota AM, Botti G: Canine mastocytoma: report of 8 cases diagnosed by fine needle cytology and clinicopathologic correlations. Acta Cytol; 2007 Jul-Aug;51(4):616-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Canine mastocytoma: report of 8 cases diagnosed by fine needle cytology and clinicopathologic correlations.
  • BACKGROUND: Mast cell proliferations are commoner in dogs than in humans; mass forming lesions in the former are apt to fine needle sampling and the obtained cytopathological picture might be informing to enhance recognition of similar proliferations in humans.
  • CASE: Clinical and cytopathologic data were collected from 8 cases of canine mastocytomas diagnosed by fine needle cytology.
  • CONCLUSION: There are marked similarities between canine and human mastocytomas, despite possible differences in the clinical course of the disease in both species.
  • Canine mastocytomas may hence be used as an animal model of a human disease and, as such, familiarity with their cytologic presentation may be useful for recognizing mast cell proliferations in humans.
  • [MeSH-major] Dog Diseases / diagnosis. Dog Diseases / pathology. Mastocytoma / diagnosis. Mastocytoma / veterinary
  • [MeSH-minor] Animals. Biopsy, Fine-Needle. Dogs. Female. Immunohistochemistry. Immunophenotyping. Lymph Nodes / pathology. Male. Mast Cells / pathology

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  • (PMID = 17718137.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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18. Fujimi K, Uehara Y, Abe S, Kawamura A, Devarajan S, Miura S, Saku K, Urata H: Homocysteine-induced oxidative stress upregulates chymase in mouse mastocytoma cells. Hypertens Res; 2010 Feb;33(2):149-54

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Homocysteine-induced oxidative stress upregulates chymase in mouse mastocytoma cells.
  • In this study, we tested whether oxidative stress upregulates mouse mast cell proteinase chymase, mouse mast cell proteinase (MMCP)-5 or MMCP-4.
  • Cultured mouse mastocytoma cells (MMC) displaying chymase-dependent Ang II-forming activity were treated with H(2)O(2) and several aminothiols with or without anti-oxidants.
  • Homocysteine increased mast cell chymase expression and activity through the mechanism of oxidative stress.
  • [MeSH-major] Chymases / genetics. Homocysteine / pharmacology. Mastocytoma / enzymology. Oxidative Stress
  • [MeSH-minor] Angiotensin II / biosynthesis. Animals. Cell Line, Tumor. Mice. RNA, Messenger / analysis. Reactive Oxygen Species / metabolism. Up-Regulation

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  • (PMID = 19960020.001).
  • [ISSN] 1348-4214
  • [Journal-full-title] Hypertension research : official journal of the Japanese Society of Hypertension
  • [ISO-abbreviation] Hypertens. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0LVT1QZ0BA / Homocysteine; 11128-99-7 / Angiotensin II; EC 3.4.21.39 / Chymases
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19. Riva F, Brizzola S, Stefanello D, Crema S, Turin L: A study of mutations in the c-kit gene of 32 dogs with mastocytoma. J Vet Diagn Invest; 2005 Jul;17(4):385-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A study of mutations in the c-kit gene of 32 dogs with mastocytoma.
  • Mutations in the intracellular juxtamembrane domain of the c-kit gene in 32 dogs with different grades of histologically confirmed mastocytoma were studied.
  • No mutations were detected in tissues constitutively expressing c-kit (cerebellum and spleen), obtained from dogs not affected by mastocytoma (controls).
  • All the substitutions were found in dogs bearing grade I or II mast cell tumors; the deletion was detected in 1 dog with grade II mastocytoma.
  • [MeSH-major] Dog Diseases / genetics. Mastocytoma / veterinary. Mutation. Proto-Oncogene Proteins c-kit / genetics

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  • (PMID = 16131001.001).
  • [ISSN] 1040-6387
  • [Journal-full-title] Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
  • [ISO-abbreviation] J. Vet. Diagn. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Neoplasm; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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20. Krishnan KR, Ownby DR: A solitary mastocytoma presenting with urticaria and angioedema in a 14-year-old boy. Allergy Asthma Proc; 2010 Nov-Dec;31(6):520-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A solitary mastocytoma presenting with urticaria and angioedema in a 14-year-old boy.
  • Mastocytosis is a rare disease that very seldom presents with urticaria but may be associated with significant morbidity and mortality if not recognized in a timely manner.
  • We are presenting a case of a 14-year-old boy who presented with urticaria and angioedema possibly caused by a solitary mastocytoma.
  • The learning points from this case are that mastocytosis should be considered in the differential diagnosis of urticaria and solitary mastocytomas may remain active into adolescence, raising concern for systemic progression.

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  • (PMID = 21708063.001).
  • [ISSN] 1539-6304
  • [Journal-full-title] Allergy and asthma proceedings
  • [ISO-abbreviation] Allergy Asthma Proc
  • [Language] ENG
  • [Publication-type] Case Reports; Clinical Conference; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.21.59 / Tryptases
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21. Leadbeater JC, Gutierrez-Nibeyro SD, Brown JA: Mastocytoma in the common carpal sheath of the digital flexor tendons of a horse. Aust Vet J; 2010 Jan;88(1-2):20-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mastocytoma in the common carpal sheath of the digital flexor tendons of a horse.
  • Thecotomy was required to fully debride the mass, which histology revealed to be a mast cell tumour.
  • At 22 months postoperatively, the horse developed mild right forelimb lameness and eosinophilic tenosynovitis because of recurrence of the mastocytoma.
  • [MeSH-major] Horse Diseases / diagnosis. Horse Diseases / surgery. Mastocytoma / veterinary. Tenosynovitis / veterinary

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  • (PMID = 20148821.001).
  • [ISSN] 1751-0813
  • [Journal-full-title] Australian veterinary journal
  • [ISO-abbreviation] Aust. Vet. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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22. Hunter MJ, Iodice MW, Pathak AK, Street MA, Helm BA: Characterization of an early signaling defect following Fc epsilonRI activation in the canine mastocytoma cell line, C2. Mol Immunol; 2009 Mar;46(6):1260-5
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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 an early signaling defect following Fc epsilonRI activation in the canine mastocytoma cell line, C2.
  • A comparison of IgE recognition by cognate receptors expressed on the C2 canine mastocytoma cell line with analogous events in a rat basophilic leukemia cell line transfected with the alpha-chain subunit of the canine high-affinity IgE receptor using flow cytometry show that canine IgE recognizes the alpha-chain of its cognate receptor on both cell lines.
  • Our study confirms the expression of functional IgE receptors in both cell lines, but receptor-mediated signaling in the C2 line only supports the early stages of downstream signaling as shown by the phosphorylation of the gamma-chain and the failure to effect the phosphorylation of Syk.
  • We propose that the identification of the precise signaling defect in C2 cells will yield useful information regarding the pathway leading to mast cell exocytosis and facilitate the restoration of the complete signaling cascade through complementation of the missing/defective signal transducer since signaling events downstream of Ca(2+) mobilization are intact as demonstrated by beta-hexosaminidase release following non-immunologic stimulation with the calcium ionophore, A23187.
  • [MeSH-major] Mast Cells / physiology. Receptors, IgE / metabolism
  • [MeSH-minor] Animals. Calcimycin / pharmacology. Cell Line, Tumor. Dogs. Exocytosis. Intracellular Signaling Peptides and Proteins / metabolism. Mastocytoma. Phosphorylation. Protein-Tyrosine Kinases / metabolism. Rats. Signal Transduction. beta-N-Acetylhexosaminidases / secretion

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  • (PMID = 19135724.001).
  • [ISSN] 1872-9142
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BBSQ/Q/2005/06706
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Receptors, IgE; 37H9VM9WZL / Calcimycin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; EC 3.2.1.52 / beta-N-Acetylhexosaminidases
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23. Schmutzler S, Bachmann L, Fuhrmann H, Schumann J: PUFA-dependent alteration of oxidative parameters of a canine mastocytoma cell line. Acta Vet Hung; 2010 Dec;58(4):453-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PUFA-dependent alteration of oxidative parameters of a canine mastocytoma cell line.
  • Mast cells play a key role in the immune response.
  • Thereby, the balance of oxidative metabolism is of importance in mast cell mediator synthesis and release.
  • Fatty acids may modify mast cell function in several ways.
  • In this study, we investigated the influence of polyunsaturated fatty acids (PUFAs) on oxidative parameters of a canine mastocytoma cell line.
  • Distinct differences between the PUFAs tested underline the impact of the unsaturation degree of fatty acids as well as the position of double bonds on mast cells.
  • [MeSH-major] DNA Damage / drug effects. Fatty Acids, Unsaturated / pharmacology. Lipid Peroxidation / drug effects. Mast Cells / drug effects. Mastocytoma / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Dogs. Oxidation-Reduction. Peptides / pharmacology. Reactive Oxygen Species / metabolism. Wasp Venoms / pharmacology

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  • (PMID = 21087915.001).
  • [ISSN] 0236-6290
  • [Journal-full-title] Acta veterinaria Hungarica
  • [ISO-abbreviation] Acta Vet. Hung.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Fatty Acids, Unsaturated; 0 / Peptides; 0 / Reactive Oxygen Species; 0 / Wasp Venoms; 72093-21-1 / mastoparan
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24. Hadzijusufovic E, Rebuzzi L, Gleixner KV, Ferenc V, Peter B, Kondo R, Gruze A, Kneidinger M, Krauth MT, Mayerhofer M, Samorapoompichit P, Greish K, Iyer AK, Pickl WF, Maeda H, Willmann M, Valent P: Targeting of heat-shock protein 32/heme oxygenase-1 in canine mastocytoma cells is associated with reduced growth and induction of apoptosis. Exp Hematol; 2008 Nov;36(11):1461-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting of heat-shock protein 32/heme oxygenase-1 in canine mastocytoma cells is associated with reduced growth and induction of apoptosis.
  • OBJECTIVE: Advanced mast cell (MC) neoplasms are usually resistant to conventional therapy.
  • Mastocytomas in dogs often behave as aggressive tumors.
  • We report that heat-shock protein 32 (Hsp32), also known as heme oxygenase-1, is a survival-enhancing molecule and new target in canine mastocytoma cells.
  • MATERIALS AND METHODS: As assessed by reverse transcriptase polymerase chain reaction, Northern blotting, immunocytochemistry, and Western blotting, primary neoplastic dog MC, and the canine mastocytoma-derived cell line C2 expressed Hsp32 mRNA and the Hsp32 protein in a constitutive manner.
  • [MeSH-major] Apoptosis / drug effects. Heme Oxygenase-1 / antagonists & inhibitors. Mastocytoma / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Dogs. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / metabolism. RNA, Messenger / analysis

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  • (PMID = 18723263.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 1.14.99.3 / Heme Oxygenase-1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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25. Rebuzzi L, Willmann M, Sonneck K, Gleixner KV, Florian S, Kondo R, Mayerhofer M, Vales A, Gruze A, Pickl WF, Thalhammer JG, Valent P: Detection of vascular endothelial growth factor (VEGF) and VEGF receptors Flt-1 and KDR in canine mastocytoma cells. Vet Immunol Immunopathol; 2007 Feb 15;115(3-4):320-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of vascular endothelial growth factor (VEGF) and VEGF receptors Flt-1 and KDR in canine mastocytoma cells.
  • In the present study, we have investigated expression of VEGF and VEGF receptors in canine mastocytomas and the canine mastocytoma cell line C2.
  • As assessed by immunostaining of tissue sections and cytospin slides, primary neoplastic mast cells (MC) and C2 cells were found to express the VEGF protein.
  • Together, canine mastocytoma cells express VEGF as well as VEGF receptors.
  • However, despite co-expression of VEGF and its receptors, VEGF is not utilized as an autocrine growth regulator by canine mastocytoma cells.
  • [MeSH-major] Dog Diseases / metabolism. Mastocytoma / veterinary. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor Receptor-1 / biosynthesis. Vascular Endothelial Growth Factor Receptor-2 / biosynthesis
  • [MeSH-minor] Animals. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Bevacizumab. Blotting, Northern / veterinary. Cell Line, Tumor. Chromones / pharmacology. Dogs. Female. Flavonoids / pharmacology. Flow Cytometry / veterinary. Immunohistochemistry / veterinary. Male. Morpholines / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / metabolism. Protein Kinase Inhibitors / pharmacology. RNA / chemistry. RNA / genetics. Reverse Transcriptase Polymerase Chain Reaction / veterinary. Sirolimus / pharmacology

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  • (PMID = 17196258.001).
  • [ISSN] 0165-2427
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Chromones; 0 / Flavonoids; 0 / Morpholines; 0 / Protein Kinase Inhibitors; 0 / Vascular Endothelial Growth Factor A; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 2S9ZZM9Q9V / Bevacizumab; 63231-63-0 / RNA; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; W36ZG6FT64 / Sirolimus
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26. Sekis I, Gerner W, Willmann M, Rebuzzi L, Tichy A, Patzl M, Thalhammer JG, Saalmüller A, Kleiter MM: Effect of radiation on vascular endothelial growth factor expression in the C2 canine mastocytoma cell line. Am J Vet Res; 2009 Sep;70(9):1141-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of radiation on vascular endothelial growth factor expression in the C2 canine mastocytoma cell line.
  • OBJECTIVE: To establish the radiosensitivity and effect of irradiation on vascular endothelial growth factor (VEGF) and VEGF receptor (VEGFR) expression in the canine mastocytoma cell line C2.
  • SAMPLE POPULATION: Canine mastocytoma cell line C2.
  • Cell survival rates decreased in a dose-dependent manner.
  • The apoptotic cell fraction had a dose-dependent increase that reached its maximum 24 to 48 hours after radiation.
  • CONCLUSIONS AND CLINICAL RELEVANCE: The C2 cell line was radiosensitive, and a fraction (up to 40%) of cells died via apoptosis in a dose-dependent manner.
  • Further studies are needed to determine whether tumor control could be improved by combining radiotherapy with VEGFR inhibitors or apoptosis-modulating agents.
  • [MeSH-major] Dog Diseases / radiotherapy. Mast-Cell Sarcoma / veterinary. Vascular Endothelial Growth Factor A / genetics
  • [MeSH-minor] Animals. Annexin A5 / genetics. Apoptosis / radiation effects. Cell Division / radiation effects. Cell Line, Tumor. Dogs. Dose-Response Relationship, Radiation. Humans. Vascular Endothelial Growth Factor Receptor-1 / genetics

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  • (PMID = 19719431.001).
  • [ISSN] 0002-9645
  • [Journal-full-title] American journal of veterinary research
  • [ISO-abbreviation] Am. J. Vet. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1
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27. Kataoka H, Sakanaka M, Semma M, Yamamoto T, Hirota S, Tanaka S, Ichikawa A: PGE2-receptor subtype EP4-dependent adherence of mastocytoma P-815 cells to matrix components in subcutaneous tissues overlaying inside surface of air pouch cavity in CDF1 mouse. Inflamm Res; 2008 Aug;57(8):362-6
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  • [Title] PGE2-receptor subtype EP4-dependent adherence of mastocytoma P-815 cells to matrix components in subcutaneous tissues overlaying inside surface of air pouch cavity in CDF1 mouse.
  • OBJECTIVES: It remains to be fully clarified how adhesion of mast cells is regulated in vivo.
  • We previously reported that PGE2-receptor EP4 stimulated the adhesion of mouse mastocytoma P-815 cells to plate-bound fibronectin.
  • [MeSH-major] Cell Adhesion / physiology. Extracellular Matrix / metabolism. Mastocytoma. Receptors, Prostaglandin E / metabolism. Subcutaneous Tissue / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cyclooxygenase Inhibitors / metabolism. Ibuprofen / metabolism. Male. Mast Cells / cytology. Mast Cells / metabolism. Mice. Mice, Inbred Strains. Naphthalenes / metabolism. Phenylbutyrates / metabolism. Receptors, Prostaglandin E, EP4 Subtype. Tetradecanoylphorbol Acetate / metabolism

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  • (PMID = 18787774.001).
  • [ISSN] 1023-3830
  • [Journal-full-title] Inflammation research : official journal of the European Histamine Research Society ... [et al.]
  • [ISO-abbreviation] Inflamm. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / 4-(4-cyano-2-(2-(4-fluoronaphthalen-1-yl)propionylamino)phenyl)butyric acid; 0 / Cyclooxygenase Inhibitors; 0 / Naphthalenes; 0 / Phenylbutyrates; 0 / Ptger4 protein, mouse; 0 / Receptors, Prostaglandin E; 0 / Receptors, Prostaglandin E, EP4 Subtype; NI40JAQ945 / Tetradecanoylphorbol Acetate; WK2XYI10QM / Ibuprofen
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28. Elders RC, Baines SJ, Catchpole B: Susceptibility of the C2 canine mastocytoma cell line to the effects of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Vet Immunol Immunopathol; 2009 Jul 15;130(1-2):11-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Susceptibility of the C2 canine mastocytoma cell line to the effects of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family, which preferentially induces apoptosis in cells that have undergone malignant transformation.
  • The aim of the current study was to investigate the effect of TRAIL on the canine C2 mastocytoma cell line to determine whether this agent might be a suitable treatment for mast cell tumors in dogs.
  • Cell metabolism was assessed using a colorimetric MTT-based assay.
  • The effect of TRAIL on the C2 cell line suggests that this cytokine might be suitable for treatment of mast cell tumors in dogs.
  • [MeSH-major] Apoptosis / drug effects. Dog Diseases / drug therapy. Mastocytoma / veterinary. Skin Neoplasms / veterinary. TNF-Related Apoptosis-Inducing Ligand / pharmacology
  • [MeSH-minor] Animals. Caspase 3 / metabolism. Caspase 7 / metabolism. Cell Line, Tumor. Cell Survival / immunology. Dogs. Flow Cytometry / veterinary. Osteoprotegerin / chemistry. Osteoprotegerin / genetics. Polymerase Chain Reaction / veterinary. Recombinant Proteins / pharmacology

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  • (PMID = 19185923.001).
  • [ISSN] 1873-2534
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Osteoprotegerin; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF11B protein, human; 0 / TNFSF10 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7
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29. Seidel A, Gueck T, Fuhrmann H: The Influence of long-chain polyunsaturated fatty acids on total lipid fatty acid composition of a canine mastocytoma cell line. J Vet Med A Physiol Pathol Clin Med; 2005 Jun;52(5):219-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Influence of long-chain polyunsaturated fatty acids on total lipid fatty acid composition of a canine mastocytoma cell line.
  • Cutaneous mast cells are considered as key immune effectors in the pathogenesis of canine atopic dermatitis (CAD).
  • The purpose of this study was to examine the effects of n6- and n3-fatty acids on the fatty acid composition of canine mastocytoma cells (C2) as a possible model for CAD.
  • Cell growth was examined for 11 days in all media.
  • Cell growth increased from days 1 to 8 and decreased thereafter in all media conditions.
  • The fatty acids supplied did not influence cell growth.
  • [MeSH-major] Dermatitis, Atopic / veterinary. Disease Models, Animal. Dog Diseases / pathology. Fatty Acids, Unsaturated / pharmacology. Inflammation Mediators / metabolism. Mast Cells / drug effects
  • [MeSH-minor] Animals. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Docosahexaenoic Acids / administration & dosage. Docosahexaenoic Acids / pharmacology. Dogs. Mastocytoma / pathology. Mastocytoma / veterinary. gamma-Linolenic Acid / administration & dosage. gamma-Linolenic Acid / pharmacology

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  • (PMID = 15943605.001).
  • [ISSN] 0931-184X
  • [Journal-full-title] Journal of veterinary medicine. A, Physiology, pathology, clinical medicine
  • [ISO-abbreviation] J Vet Med A Physiol Pathol Clin Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fatty Acids, Unsaturated; 0 / Inflammation Mediators; 25167-62-8 / Docosahexaenoic Acids; 78YC2MAX4O / gamma-Linolenic Acid
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30. Schmidt CS, Bentz ML: Congenital smooth muscle hamartoma: the importance of differentiation from melanocytic nevi. J Craniofac Surg; 2005 Sep;16(5):926-9
MedlinePlus Health Information. consumer health - Skin Conditions.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The clinical differential diagnosis of CSMH includes congenital melanocytic (pigmented) nevus, Becker's melanosis, solitary mastocytoma, piloleiomyoma, café-au-lait spots, and nevus pilosus.
  • Differentiating CSMH from a congenital melanocytic nevus avoids the unnecessary excision of this benign condition.
  • [MeSH-minor] Cafe-au-Lait Spots / diagnosis. Diagnosis, Differential. Humans. Infant. Leiomyoma / diagnosis. Male. Mastocytoma / diagnosis. Melanosis / diagnosis. Nevus / diagnosis

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  • (PMID = 16192884.001).
  • [ISSN] 1049-2275
  • [Journal-full-title] The Journal of craniofacial surgery
  • [ISO-abbreviation] J Craniofac Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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31. Jakab C, Szász AM, Kulka J, Schaff Z, Rusvai M, Németh T, Gálfi P: Cutaneous mast cell tumour within a lipoma in a boxer. Acta Vet Hung; 2009 Jun;57(2):263-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cutaneous mast cell tumour within a lipoma in a boxer.
  • This report describes a case of a canine cutaneous grade I mast cell tumour which developed within a lipoma in the right axillar region of an 8-year-old male Boxer.
  • Immunohistologically, the neoplastic mast cells were positive for serotonin, CD45 vimentin and p53, and negative for lysozyme, CD3 and CD79a expression.
  • The proliferation index of the mast cell tumour based on the Ki-67 antigen was 6.1%.
  • Between the benign neoplastic lipocytes and mastocytoma tumour cells intratumoural microvessels were detected by immunohistochemical staining using CD31 and claudin-5 as markers for vascular endothelium.
  • [MeSH-major] Dog Diseases / pathology. Lipoma / veterinary. Mastocytoma / veterinary. Skin Neoplasms / veterinary

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  • (PMID = 19584039.001).
  • [ISSN] 0236-6290
  • [Journal-full-title] Acta veterinaria Hungarica
  • [ISO-abbreviation] Acta Vet. Hung.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Hungary
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32. Bağriaçik EÜ, Uslu K, Yurtçu E, Stefek M, Karasu C: Stobadine inhibits doxorubicin-induced apoptosis through a caspase-9 dependent pathway in P815 mastocytoma cells. Cell Biol Int; 2007 Sep;31(9):979-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stobadine inhibits doxorubicin-induced apoptosis through a caspase-9 dependent pathway in P815 mastocytoma cells.
  • Pretreating cells with stobadine significantly increased cell viability and decreased apoptosis rate.
  • [MeSH-major] Apoptosis / drug effects. Carbolines / pharmacology. Caspase 9 / metabolism. Doxorubicin / pharmacology. Mastocytoma / enzymology. Mastocytoma / pathology

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  • (PMID = 17481927.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Carbolines; 0 / Caspase Inhibitors; 80168379AG / Doxorubicin; EC 3.4.22.- / Caspase 9; WYQ7N0BPYC / Acetylcysteine; Y0EA50IJ3V / dicarbine
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33. Singalavanija S, Limpongsanurak W: Cutaneous mastocytosis in Thai children. J Med Assoc Thai; 2008 Oct;91 Suppl 3:S143-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Mastocytosis is a disorder of mast cells proliferation within various organs, most commonly in the skin.
  • The disease more commonly appears during infancy than adult.
  • There were 45 cases (90%) of urticaria pigmentosa, 3 cases (6%) of mastocytoma and 2 cases (4%) of diffuse cutaneous mastocytosis.
  • Most of the children were healthy, except the one who had germ cell ovarian tumor Skin biopsies were performed in all cases and revealed mast cells infiltrate in the dermis.
  • Oral mast cell stabilizers were given in 6 patients (12%) and topical corticosteroids in 15 patients (30%).
  • CONCLUSION: Cutaneous mastocytosis is a benign disease in children without systemic involvement.
  • [MeSH-major] Mast Cells / pathology. Mastocytoma, Skin / diagnosis. Urticaria Pigmentosa / diagnosis

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  • (PMID = 19253510.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Histamine Antagonists; 9PHQ9Y1OLM / Prednisolone
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34. Bulat V, Mihić LL, Situm M, Buljan M, Blajić I, Pusić J: Most common clinical presentations of cutaneous mastocytosis. Acta Clin Croat; 2009 Mar;48(1):59-64
Genetic Alliance. consumer health - Cutaneous mastocytosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The term mastocytosis is referred to as an array of uncommon, usually sporadic, heterogeneous clinical illnesses that result from the hyperplasia of tissue mast cells.
  • The characteristic presentation of mastocytosis consists of cutaneous manifestations: either a solitary mastocytoma, urticaria pigmentosa, or less commonly, diffuse cutaneous mastocytosis.
  • Mastocytosis may also be manifested as mastocytoma, a rare, benign, pediatric tumor that results from hyperplasia of mast cells in papillary dermis in the first few weeks of life.
  • The prognosis for the majority of pediatric patients with urticaria pigmentosa is extremely good, and over half of cases clear completely by adolescence, while those with aggressive systemic mastocytosis or mast cell leukemia show a progressive course, usually with a fatal outcome.

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  • (PMID = 19623875.001).
  • [ISSN] 0353-9466
  • [Journal-full-title] Acta clinica Croatica
  • [ISO-abbreviation] Acta Clin Croat
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Croatia
  • [Number-of-references] 17
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35. Zhang X, Mei W, Zhang L, Yu H, Zhao X, Fan X, Qian G, Ge S: Co-expression of P1A35-43/beta2m fusion protein and co-stimulatory molecule CD80 elicits effective anti-tumor immunity in the P815 mouse mastocytoma tumor model. Oncol Rep; 2009 Nov;22(5):1213-20

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  • [Title] Co-expression of P1A35-43/beta2m fusion protein and co-stimulatory molecule CD80 elicits effective anti-tumor immunity in the P815 mouse mastocytoma tumor model.
  • A strong CTL response is dependent upon a high level of expression of specific class I major histocompatibility complex (MHC)/peptide complexes at the cell surface.
  • In this study, we modified the P1A tumor cell vaccine by addition of the tumor-associated epitope (TAE)-linked beta2m molecule and co-stimulatory molecule CD80 to improve the efficiency in the application of the vaccine.
  • P815 cell lines stably expressing P1A35-43-linked beta2m molecule and/or CD80 were established after transfection, by selection under G418.
  • Administration of these inactivated tumor cell vaccines allowed the TAE-specific CD8+ T cell responses to be examined in vivo.
  • Our results indicate that immunization with P815 cells expressing both the P1A35-43-linked beta2m molecule and the murine CD80 gene elicited a significantly stronger antitumor immune response than the single-modified tumor cell vaccines (expressing either P1A35-43-linked beta2m or CD80 alone).
  • These findings support the feasibility and effectiveness of developing a dual-modified tumor cell vaccine consisting of the epitope-linked beta2m molecule and a co-stimulatory molecule.
  • [MeSH-major] Antigens, CD80 / immunology. Antigens, Neoplasm / immunology. Cancer Vaccines / therapeutic use. Mastocytoma / immunology. Mastocytoma / therapy. beta 2-Microglobulin / immunology

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  • (PMID = 19787242.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Recombinant Fusion Proteins; 0 / beta 2-Microglobulin; 0 / tumor rejection antigen P815A, mouse; 82115-62-6 / Interferon-gamma
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36. Martínez-Lage JF, Niguez BF, Pérez-Espejo MA, Almagro MJ, Maeztu C: Midline cutaneous lumbosacral lesions: not always a sign of occult spinal dysraphism. Childs Nerv Syst; 2006 Jun;22(6):623-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PATIENTS AND METHODS: The pathological diagnosis of the masses was plexiform neurofibroma and mastocytoma, respectively.
  • Plexiform neurofibroma and skin mastocytoma are very rare indeed in this spinal location.
  • [MeSH-major] Mastocytoma / diagnosis. Neurofibroma / diagnosis

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  • (PMID = 16453111.001).
  • [ISSN] 0256-7040
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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37. Gamlem H, Nordstoga K, Glattre E: Canine neoplasia--introductory paper. APMIS Suppl; 2008;(125):5-18

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the age group 2-3.99 years histiocytoma was still the largest group in males, but was surpassed by benign epithelial skin tumours in females.
  • After the age of 4 years, benign epithelial skin tumours constituted the greatest circumscribed group in males, and mammary tumours in females, although the summated other tumours, not explained in this survey, dominated overall in males.
  • While mastocytoma was the most common tumour and non-Hodgkin's lymphoma the second most common during the two first years of life in females, the situation was reversed in males.
  • As benign vascular tumours are incompletely reported to the human Cancer Registry, no dependable comparison may be made, but malignant vascular tumours have been on the rise during the last decades in the Norwegian human population, more so in men then in women.

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  • (PMID = 19385278.001).
  • [ISSN] 0903-465X
  • [Journal-full-title] APMIS. Supplementum
  • [ISO-abbreviation] APMIS Suppl.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Denmark
  • [Number-of-references] 55
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38. Horny HP, Sotlar K, Valent P: Mastocytosis: state of the art. Pathobiology; 2007;74(2):121-32
Genetic Alliance. consumer health - Mast cell disease.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Mastocytosis is a neoplastic disease involving mast cells (MC) and their CD34+ progenitors.
  • (1) Cutaneous mastocytosis (CM), a benign disease in which MC infiltration is confined to the skin, is preferentially seen in young children and exhibits a marked tendency to regress spontaneously. (2) Systemic mastocytosis (SM) which is commonly diagnosed in adults and includes four major subtypes: (i) indolent SM (ISM, the most common form involving mainly skin and bone marrow);.
  • (ii) a unique subcategory termed SM with an associated non-mast cell clonal hematological disease (SM-AHNMD);.
  • (iii) aggressive SM usually presenting without skin lesions, and (iv) MC leukemia, probably representing the rarest variant of human leukemias. (3) The extremely rare localized extracutaneous MC neoplasms, either presenting as malignancy (MC sarcoma) or as benign tumor termed extracutaneous mastocytoma.
  • Most patients, in particular those with CM and ISM, remain in an indolent stage over many years or even decades, while others, in particular those with aggressive SM, SM-AHNMD, or mast cell leukemia, show a progressive course, usually with a fatal outcome.
  • [MeSH-major] Bone Marrow / pathology. Mast Cells / pathology. Mastocytosis / diagnosis. Skin / pathology
  • [MeSH-minor] Antigens, CD2 / analysis. Antigens, CD34 / analysis. Biopsy. Diagnosis, Differential. Disease Progression. Humans. Interleukin-2 Receptor alpha Subunit / analysis. Leukemia, Mast-Cell / diagnosis. Leukemia, Mast-Cell / pathology. Mast-Cell Sarcoma / diagnosis. Mast-Cell Sarcoma / pathology. Mastocytosis, Cutaneous / diagnosis. Mastocytosis, Cutaneous / pathology. Mastocytosis, Systemic / diagnosis. Mastocytosis, Systemic / pathology. Mutation. Practice Guidelines as Topic. Prognosis. Proto-Oncogene Proteins c-kit / analysis. Proto-Oncogene Proteins c-kit / genetics. Tryptases / analysis. World Health Organization

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  • (PMID = 17587883.001).
  • [ISSN] 1015-2008
  • [Journal-full-title] Pathobiology : journal of immunopathology, molecular and cellular biology
  • [ISO-abbreviation] Pathobiology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD2; 0 / Antigens, CD34; 0 / Interleukin-2 Receptor alpha Subunit; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.21.59 / Tryptases
  • [Number-of-references] 62
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39. Seledtsov VI, Seledtsova GV, Samarin DM, Senyukov VV, Poveschenko OV, Felde MA, Kozlov VA: Erythroid cells in suppressing leukemia cell growth. Leuk Lymphoma; 2005 Sep;46(9):1353-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Erythroid cells in suppressing leukemia cell growth.
  • This paper indicates that murine nucleated erythroid cells (EC) are able to reduce, in a dose-dependent manner, the proliferation of both L1210 lymphoma and P815 mastocytoma cells and that the leukemia cell growth inhibitory activity of unseparated bone marrow (BM) cells may be markedly augmented by their short-term culturing with erythropoietin (Epo).
  • These results raise the intriguing possibility to utilize erythropoesis-stimulating, therapeutic strategies with the purpose of inhibiting leukemia cell growth in the body.
  • [MeSH-minor] Animals. Bone Marrow Cells / physiology. Cell Division / drug effects. Cells, Cultured. Erythropoietin / pharmacology. Leukemia L1210 / pathology. Mice. Mice, Inbred Strains. Tumor Cells, Cultured

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  • (PMID = 16109614.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 11096-26-7 / Erythropoietin
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40. Akoglu G, Erkin G, Cakir B, Boztepe G, Sahin S, Karaduman A, Atakan N, Akan T, Kolemen F: Cutaneous mastocytosis: demographic aspects and clinical features of 55 patients. J Eur Acad Dermatol Venereol; 2006 Sep;20(8):969-73
Genetic Alliance. consumer health - Cutaneous mastocytosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Mastocytosis is a rare, heterogeneous group of disorder with abnormal increase of mast cells in one or more organ systems.
  • RESULTS: Of the 22 females and 33 males, 80% had urticaria pigmentosa/maculopapular CM and 20% had mastocytoma.
  • CONCLUSION: Clinical presentations of urticaria pigmentosa/maculopapular CM and mastocytoma are similar regarding gender, age of onset, age of diagnosis, and presence of Darier's sign and history of bulla.
  • In contrast to mastocytoma, urticaria pigmentosa/maculopapular CM lesions were frequently located on trunk together with extremities.

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  • (PMID = 16922947.001).
  • [ISSN] 0926-9959
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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41. Mojahidi S, Rakib el M, Sekkak H, Abouricha S, Benchat N, Mousse HA, Zyad A: Synthesis and in-vitro cytotoxic evaluation of novel pyridazin-4-one derivatives. Arch Pharm (Weinheim); 2010 May;343(5):310-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Some of these compounds exhibited in-vitro cytotoxic activity with moderate to excellent growth inhibition against the murine P815 mastocytoma cell line.
  • Compound 5b showed an important cytotoxic activity against cell line P815 (IC(50 )= 0.40 microg/mL).
  • [MeSH-major] Antineoplastic Agents / chemical synthesis. Antineoplastic Agents / pharmacology. Cell Proliferation / drug effects. Pyridazines / chemical synthesis. Pyridazines / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Screening Assays, Antitumor / methods. Mice. Molecular Structure. Structure-Activity Relationship

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  • (PMID = 20222064.001).
  • [ISSN] 1521-4184
  • [Journal-full-title] Archiv der Pharmazie
  • [ISO-abbreviation] Arch. Pharm. (Weinheim)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyridazines
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42. Masserdotti C, Bonfanti U, De Lorenzi D, Tranquillo M, Zanetti O: Cytologic features of testicular tumours in dog. J Vet Med A Physiol Pathol Clin Med; 2005 Sep;52(7):339-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cytological diagnosis was consistent with seminoma in 20 cases, sertolioma in 16 cases, Leydig cell tumours in 50 cases and mastocytoma in one case.
  • Cytology provided a sensitivity of 95% for seminoma, 88% for sertolioma and 96% for Leydig cell tumours.
  • [MeSH-minor] Animals. Dogs. Italy / epidemiology. Leydig Cell Tumor / pathology. Leydig Cell Tumor / veterinary. Male. Mastocytoma / pathology. Mastocytoma / veterinary. Predictive Value of Tests. Seminoma / pathology. Seminoma / veterinary. Sensitivity and Specificity. Sertoli Cell Tumor / pathology. Sertoli Cell Tumor / veterinary

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  • (PMID = 16109100.001).
  • [ISSN] 0931-184X
  • [Journal-full-title] Journal of veterinary medicine. A, Physiology, pathology, clinical medicine
  • [ISO-abbreviation] J Vet Med A Physiol Pathol Clin Med
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Germany
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43. Purnell B, Sato A, O'kelley A, Price C, Summerville K, Hudson S, O'hare C, Kiakos K, Asao T, Lee M, Hartley JA: DNA interstrand crosslinking agents: synthesis, DNA interactions, and cytotoxicity of dimeric achiral seco-amino-CBI and conjugates of achiral seco-amino-CBI with pyrrolobenzodiazepine (PBD). Bioorg Med Chem Lett; 2006 Nov 1;16(21):5677-81
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  • Compounds 11 and 12 demonstrated enhanced cytotoxicity over the monomer counterparts against the growth of P815 murine mastocytoma cells in culture.

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  • (PMID = 16919946.001).
  • [ISSN] 0960-894X
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cross-Linking Reagents; 0 / Cyclopropanes; 0 / Indoles; 0 / Pyrroles; 0 / pyrrolo(2,1-c)(1,4)benzodiazepine; 12794-10-4 / Benzodiazepines; 496-15-1 / indoline; 9007-49-2 / DNA; 99TB643425 / cyclopropane
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44. Litviakov NV, Buldakov MA, Cherdyntseva NV, Rostov VV, Klimov AI, Bol'shakov MA: [Effect of impulse-intermittent ultrahigh frequency irradiation on synthesis of nucleic acids in tumor cells]. Radiats Biol Radioecol; 2005 Jul-Aug;45(4):460-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effect of impulse-intermittent ultrahigh frequency irradiation on synthesis of nucleic acids in tumor cells].
  • In this work is shown that the repetitive high power microwaves is able to exert an inhibitory influence on the process of DNA and RNA syntheses in tumor cells of P-815 mastocytoma.
  • High power microwave pulses inhibit the process of transcription in tumor cells.
  • This indicates that the repetitive high power microwaves are not able to initiate single-filament rupture in DNA of tumor cells.

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  • (PMID = 16209193.001).
  • [ISSN] 0869-8031
  • [Journal-full-title] Radiatsionnaia biologiia, radioecologiia
  • [ISO-abbreviation] Radiats Biol Radioecol
  • [Language] RUS
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Nucleic Acids
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45. Lin TY, Bear M, Du Z, Foley KP, Ying W, Barsoum J, London C: The novel HSP90 inhibitor STA-9090 exhibits activity against Kit-dependent and -independent malignant mast cell tumors. Exp Hematol; 2008 Oct;36(10):1266-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The novel HSP90 inhibitor STA-9090 exhibits activity against Kit-dependent and -independent malignant mast cell tumors.
  • The purpose of this study was to evaluate a novel HSP90 inhibitor, STA-9090, against wild-type (WT) and mutant Kit in canine bone marrow-derived cultured mast cells (BMCMCs), malignant mast cell lines, and fresh malignant mast cells.
  • MATERIALS AND METHODS: BMCMCs, cell lines, and fresh malignant mast cells were treated with STA-9090, 17-AAG, and SU11654 and evaluated for loss in cell viability, cell death, alterations in HSP90 and Kit expression/signaling, and Kit mutation.
  • STA-9090 activity was tested in a canine mastocytoma xenograft model.
  • RESULTS: Treatment of BMCMCs, cell lines, and fresh malignant cells with STA-9090 induced growth inhibition, apoptosis that was caspase-3/7-dependent, and downregulation of phospho/total Kit and Akt, but not extracellular signal-regulated kinase (ERK) or phosphoinositide-3 kinase (PI-3K).
  • Loss of Kit cell-surface expression was also observed.
  • Furthermore, STA-9090 exhibited superior activity to 17-AAG and SU11654, and was effective against malignant mast cells expressing either WT or mutant Kit.
  • Lastly, STA-9090 inhibited tumor growth in a canine mastocytoma mouse xenograft model.
  • CONCLUSIONS: STA-9090 exhibits broad activity against mast cells expressing WT or mutant Kit, suggesting it may be an effective agent in the clinical setting against mast cell malignancies.

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  • [Cites] Exp Hematol. 1999 Apr;27(4):689-97 [10210327.001]
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  • (PMID = 18657349.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA093807; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NCATS NIH HHS / TR / UL1 TR000090; United States / NCI NIH HHS / CA / R01 CA93807
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA Primers; 0 / HSP90 Heat-Shock Proteins; 0 / STA 9090; 0 / Triazoles; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Other-IDs] NLM/ NIHMS522755; NLM/ PMC3837096
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46. Nishikawa H, Wakano K, Kitani S: Inhibition of NADPH oxidase subunits translocation by tea catechin EGCG in mast cell. Biochem Biophys Res Commun; 2007 Oct 19;362(2):504-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of NADPH oxidase subunits translocation by tea catechin EGCG in mast cell.
  • We studied the effect of catechins, mainly EGCG, on the activation of mast cell line canine cutaneous mastocytoma cells (CM-MC).
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Cell Membrane / drug effects. Cell Membrane / metabolism. Cells, Cultured. Cytosol / drug effects. Cytosol / metabolism. Dose-Response Relationship, Drug. Humans. Mast Cells / drug effects. Mast Cells / enzymology. Mast Cells / metabolism. Neutrophils / cytology. Neutrophils / drug effects. Neutrophils / metabolism. Onium Compounds / pharmacology. Phosphoproteins / metabolism. Protease Inhibitors / pharmacology. Protein Subunits / metabolism. Protein Transport / drug effects. Reactive Oxygen Species / metabolism. Time Factors. beta-N-Acetylhexosaminidases / secretion. p-Methoxy-N-methylphenethylamine / pharmacology

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  • (PMID = 17707774.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Onium Compounds; 0 / Phosphoproteins; 0 / Protease Inhibitors; 0 / Protein Subunits; 0 / Reactive Oxygen Species; 0 / Tea; 0 / neutrophil cytosol factor 40K; 0 / neutrophil cytosol factor 67K; 4091-50-3 / p-Methoxy-N-methylphenethylamine; 6HJ411TU98 / diphenyleneiodonium; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 1.6.3.1 / NADPH Oxidase; EC 3.2.1.52 / beta-N-Acetylhexosaminidases
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47. Gück T, Fuhrmann H: [Pathobiochemical importance of phospholipases for the release of mast cell mediators]. Dtsch Tierarztl Wochenschr; 2005 Nov;112(11):404-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pathobiochemical importance of phospholipases for the release of mast cell mediators].
  • We investigated the influence of polyunsaturated fatty acids on the activity of the cytosolic phospholipase A2 (cPLA2) in the canine mastocytoma cell line C2 as a model for canine atopic dermatitis (CAD).
  • [MeSH-major] Dermatitis, Atopic / veterinary. Dog Diseases / pathology. Fatty Acids, Unsaturated / pharmacology. Inflammation Mediators / metabolism. Mast Cells / metabolism. Phospholipases / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease Models, Animal. Dogs. Mastocytoma / pathology. Mastocytoma / veterinary

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  • (PMID = 16366033.001).
  • [ISSN] 0341-6593
  • [Journal-full-title] DTW. Deutsche tierärztliche Wochenschrift
  • [ISO-abbreviation] DTW. Dtsch. Tierarztl. Wochenschr.
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fatty Acids, Unsaturated; 0 / Inflammation Mediators; EC 3.1.- / Phospholipases
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48. Rossbach K, Stark H, Sander K, Leurs R, Kietzmann M, Bäumer W: The histamine H receptor as a new target for treatment of canine inflammatory skin diseases. Vet Dermatol; 2009 Oct;20(5-6):555-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To determine whether canine mast cells are susceptible to histamine H(4) receptor-mediated reactions, effects of clobenpropit and VUF 8430 were tested in canine mastocytoma cells (C2).
  • Neither VUF 8430, nor clobenpropit (up to 10 micromol/L) led to a modulation of histamine concentration in supernatants of canine mastocytoma cells, whereas mastoparan, used as a positive control, enhanced histamine concentration in supernatants.
  • [MeSH-minor] Animals. Calcium / metabolism. Cell Line. Dogs. Dose-Response Relationship, Drug. Female. Guanidines / pharmacology. Histamine / pharmacology. Histamine Agonists / pharmacology. Histamine Antagonists / pharmacology. Imidazoles / pharmacology. Inflammation / chemically induced. Inflammation / drug therapy. Inflammation / physiopathology. Inflammation / veterinary. Male. Mastocytoma. Mice. Mice, Inbred BALB C. Peptides / pharmacology. Thiourea / analogs & derivatives. Thiourea / pharmacology. Wasp Venoms / pharmacology

  • MedlinePlus Health Information. consumer health - Skin Conditions.
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  • (PMID = 20178494.001).
  • [ISSN] 1365-3164
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 1-((5-chloro-1H-indol-2-yl)carbonyl)-4-methylpiperazine; 0 / Guanidines; 0 / Histamine Agonists; 0 / Histamine Antagonists; 0 / Imidazoles; 0 / Indoles; 0 / Peptides; 0 / Piperazines; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Histamine; 0 / S-(2-guanidylethyl)isothiourea; 0 / Wasp Venoms; 145231-45-4 / clobenpropit; 72093-21-1 / mastoparan; 820484N8I3 / Histamine; GYV9AM2QAG / Thiourea; SY7Q814VUP / Calcium
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49. Bai XF, Liu JQ, Joshi PS, Wang L, Yin L, Labanowska J, Heerema N, Zheng P, Liu Y: Different lineages of P1A-expressing cancer cells use divergent modes of immune evasion for T-cell adoptive therapy. Cancer Res; 2006 Aug 15;66(16):8241-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Different lineages of P1A-expressing cancer cells use divergent modes of immune evasion for T-cell adoptive therapy.
  • Tumor evasion of T-cell immunity remains a significant obstacle to adoptive T-cell therapy.
  • It is unknown whether the mode of immune evasion is dictated by the cancer cells or by the tumor antigens.
  • Taking advantage of the fact that multiple lineages of tumor cells share the tumor antigen P1A, we adoptively transferred transgenic T cells specific for P1A (P1CTL) into mice with established P1A-expressing tumors, including mastocytoma P815, plasmocytoma J558, and fibrosarcoma Meth A.
  • Analysis of the status of the tumor antigen revealed that all J558 tumors underwent antigenic drift whereas all P815 tumors experienced antigenic loss.
  • Our data showed that, in spite of their shared tumor antigen, different lineages of cancer cells use different mechanisms to evade T-cell therapy.
  • [MeSH-major] Antigens, Neoplasm / genetics. Immunotherapy, Adoptive / methods. Receptors, Antigen, T-Cell / genetics. T-Lymphocytes / immunology. T-Lymphocytes / transplantation
  • [MeSH-minor] Animals. Apoptosis. Cell Division. Cell Survival. DNA Primers. Humans. Mice. Mice, Inbred BALB C. Mice, Transgenic. Polymerase Chain Reaction. Spleen / transplantation

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  • (PMID = 16912204.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA58033; United States / NCI NIH HHS / CA / R21CA116678
  • [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 / Antigens, Neoplasm; 0 / DNA Primers; 0 / Receptors, Antigen, T-Cell; 0 / tumor rejection antigen P815A, mouse
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50. El Kodadi M, Benamar M, Ibrahim B, Zyad A, Malek F, Touzani R, Ramdani A, Melhaoui A: New synthesis of two tridentate bipyrazolic compounds and their cytotoxic activity tumor cell lines. Nat Prod Res; 2007 Sep;21(11):947-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New synthesis of two tridentate bipyrazolic compounds and their cytotoxic activity tumor cell lines.
  • The evaluation of the cytotoxic properties in vitro of these ligands, was examined on two tumor cell lines - P815 (mastocytome murine) and Hep (carcinoma of human larynx).
  • The concentration required to induce 50% of lysis (IC(50)) was more pronounced against P815 cell line (IC(50): 39.42 microg mL(-1) for the compound 1 and 97.74 microg mL(-1) for the compound 2) than the Hep cell line (IC(50): 83.49 microg mL(-1) for compound 1 and 185.30 microg mL(-1) for compound 2).
  • [MeSH-minor] Animals. Cell Survival / drug effects. Drug Screening Assays, Antitumor. Humans. Inhibitory Concentration 50. Mice. Molecular Structure. Nuclear Magnetic Resonance, Biomolecular. Structure-Activity Relationship

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  • (PMID = 17691042.001).
  • [ISSN] 1478-6419
  • [Journal-full-title] Natural product research
  • [ISO-abbreviation] Nat. Prod. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-(bis((3,5-dimethyl-1H-pyrazole-1-yl)methyl)amino)butane-1-ol; 0 / Antineoplastic Agents; 0 / Pyrazoles; 0 / ethyl-1-(((2-hydroxyethyl)((3-(ethoxycarbonyl)-5-methyl-1H-pyrazole-1-yl)methyl)amino)methyl)-5-methyl-1H-pyrazole-3-carboxylate
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51. Briley LD, Phillips CM: Cutaneous mastocytosis: a review focusing on the pediatric population. Clin Pediatr (Phila); 2008 Oct;47(8):757-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cutaneous mastocytosis can be divided into 4 different clinical variants--urticaria pigmentosa, solitary mastocytoma, diffuse cutaneous mastocytosis, and telangiectasia macularis eruptiva perstans.
  • Skin findings are often accompanied by symptoms secondary to mast cell release of mediators.
  • This article will review each of the 4 clinical presentations focusing on pediatric-onset of disease while reviewing the literature.

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  • (PMID = 18502981.001).
  • [ISSN] 0009-9228
  • [Journal-full-title] Clinical pediatrics
  • [ISO-abbreviation] Clin Pediatr (Phila)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 14
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52. Helgason CD: Culture of primary adherent cells and a continuously growing nonadherent cell line. Methods Mol Biol; 2005;290:1-12

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Culture of primary adherent cells and a continuously growing nonadherent cell line.
  • Cell culture is an invaluable tool for investigators in numerous fields.
  • The purpose of this chapter is to explain the basic principles of cell culture using the maintenance of a nonadherent cell line, the P815 mouse mastocytoma cell line, and the isolation and culture of adherent primary mouse embryonic fibroblasts (MEFs) as examples.
  • Procedures for thawing, culture, determination of cell numbers and viability, and cryopreservation are described.
  • [MeSH-major] Cell Adhesion. Cell Culture Techniques / methods
  • [MeSH-minor] Animals. Cell Line. Cryopreservation. Embryo, Mammalian / cytology. Fibroblasts / cytology. Mice

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  • (PMID = 15361651.001).
  • [ISSN] 1064-3745
  • [Journal-full-title] Methods in molecular biology (Clifton, N.J.)
  • [ISO-abbreviation] Methods Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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53. Harris AL, Ryan JJ, Farrell N: Biological consequences of trinuclear platinum complexes: comparison of [[trans-PtCl(NH3)2]2mu-(trans-Pt(NH3)2(H2N(CH2)6-NH2)2)]4+ (BBR 3464) with its noncovalent congeners. Mol Pharmacol; 2006 Feb;69(2):666-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • All compounds induce caspase-dependent apoptosis in both primary mast cells and transformed mastocytomas, although with a smaller IC(50) value in the transformed cells.
  • In cells deficient in either the tumor suppressor proteins p53 or Bax, apoptosis was least affected in the case of II, but in all cases the effect of p53 deficiency was greater than that of Bax.
  • Cellular accumulation was enhanced in mastocytomas over primary mast cells, suggesting a mechanism for enhancement of tumor cell selectivity.
  • [MeSH-minor] Animals. Apoptosis. Caspases / metabolism. Enzyme Activation. Mast Cells / drug effects. Mast Cells / enzymology. Mice. Mice, Inbred C57BL. Tumor Suppressor Protein p53 / metabolism. bcl-2-Associated X Protein / metabolism

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  • (PMID = 16275707.001).
  • [ISSN] 0026-895X
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / 1R01-AI43433; United States / NCI NIH HHS / CA / 1R01-CA91839; United States / NCI NIH HHS / CA / CA78754
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BBR 3464; 0 / Organoplatinum Compounds; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; EC 3.4.22.- / Caspases
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54. Zhang XQ, Mei WH, Qian GX: [Activity analysis of human beta β2-microglobulin gene promoter in P815 cells]. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi; 2005 Nov;21(6):672-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A mouse mastocytoma cell line P815 was transiently and stably transfected with the plasmid containing human beta2m gene promoter and enhanced green fluorescence protein(EGFP) gene.
  • There was no difference in the fluorescence positive cell rate between the IFN-gamma-treated group and the control group.
  • CONCLUSION: Human beta2m gene promoter is active in mouse mastocytoma P815 cells.
  • [MeSH-minor] Animals. Base Sequence. Cell Line, Tumor. Flow Cytometry. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Humans. Interferon-gamma / pharmacology. Mastocytoma / metabolism. Mice. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction. Sequence Homology, Nucleic Acid. Transfection

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  • (PMID = 16256022.001).
  • [ISSN] 1007-8738
  • [Journal-full-title] Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
  • [ISO-abbreviation] Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / beta 2-Microglobulin; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins; 82115-62-6 / Interferon-gamma
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55. Peter B, Hadzijusufovic E, Blatt K, Gleixner KV, Pickl WF, Thaiwong T, Yuzbasiyan-Gurkan V, Willmann M, Valent P: KIT polymorphisms and mutations determine responses of neoplastic mast cells to bafetinib (INNO-406). Exp Hematol; 2010 Sep;38(9):782-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] KIT polymorphisms and mutations determine responses of neoplastic mast cells to bafetinib (INNO-406).
  • OBJECTIVE: Advanced systemic mastocytosis (SM) is characterized by uncontrolled growth of neoplastic mast cells (MC) and drug resistance.
  • MATERIALS AND METHODS: We determined the effects of the multikinase inhibitor INNO-406 (bafetinib) on primary neoplastic MC, the canine mastocytoma cell line C2, the human MC leukemia cell line HMC-1.1 bearing the KIT mutant V560G, and HMC-1.2 cells harboring KIT V560G and KIT D816V.
  • In human MC, the KIT D816V mutant introduces resistance, and in canine mastocytomas, an exon 11 polymorphism may be indicative of resistance against INNO-406.
  • [MeSH-major] Drug Resistance, Neoplasm. Mast Cells. Mastocytosis, Systemic. Mutation, Missense. Polymorphism, Genetic. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-kit / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / metabolism. Pyrimidines / pharmacology

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  • (PMID = 20685234.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 859212-16-1 / bafetinib; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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56. Burnham DK, Keall SN, Nelson NJ, Daugherty CH: T cell function in tuatara (Sphenodon punctatus). Comp Immunol Microbiol Infect Dis; 2005 May;28(3):213-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T cell function in tuatara (Sphenodon punctatus).
  • Previous studies of the immune system of the tuatara did not assess T cell function.
  • We analyzed T cell function among six captive tuatara by assessing concanavalin A (Con A), phytohemagglutinin (PHA) and mixed lymphocyte reaction (MLR) induced T cell proliferation.
  • However, Con A activated lymphocytes were not cytotoxic for a xenogeneic murine mastocytoma cell line (P815).
  • [MeSH-minor] Animals. Cell Proliferation. Concanavalin A / immunology. Female. Lymphocyte Activation / immunology. Lymphocyte Culture Test, Mixed. Male. Phytohemagglutinins / immunology

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  • (PMID = 15857660.001).
  • [ISSN] 0147-9571
  • [Journal-full-title] Comparative immunology, microbiology and infectious diseases
  • [ISO-abbreviation] Comp. Immunol. Microbiol. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Phytohemagglutinins; 11028-71-0 / Concanavalin A
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57. Olver S, Apte S, Baz A, Kienzle N: The duplicitous effects of interleukin 4 on tumour immunity: how can the same cytokine improve or impair control of tumour growth? Tissue Antigens; 2007 Apr;69(4):293-8
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  • Here, we summarise some of the murine tumour models used over the past two decades to assess the impact of IL-4 on tumour immunity, with emphasis on the effects of IL-4 on the tumour-induced CD8 T-cell response.
  • These data are compared with our own recent studies showing that IL-4 impairs CD8+ T-cell-mediated immunity against the mastocytoma cell line P815 expressing the immunogenic HLA-CW3 gene; moreover, we hypothesise that quantitative and qualitative differences in the HLA-CW3-induced CD8+ T-cell response impair control of tumour growth and aid the development of secondary tumours.
  • We conclude that the duplicitous effects of IL-4 on tumour immunity depend on the type of effector cell (adaptive/innate) mediating tumour clearance and whether tumour growth depends on stromal infrastructure.

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  • (PMID = 17389011.001).
  • [ISSN] 0001-2815
  • [Journal-full-title] Tissue antigens
  • [ISO-abbreviation] Tissue Antigens
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines; 0 / HLA-C Antigens; 207137-56-2 / Interleukin-4
  • [Number-of-references] 44
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58. Demehri S, Corbin A, Loriaux M, Druker BJ, Deininger MW: Establishment of a murine model of aggressive systemic mastocytosis/mast cell leukemia. Exp Hematol; 2006 Mar;34(3):284-8
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  • [Title] Establishment of a murine model of aggressive systemic mastocytosis/mast cell leukemia.
  • Aggressive systemic mastocytosis (ASM) and mast cell leukemia (MCL) are rare but devastating diseases, for which no effective specific therapy is currently available.
  • To facilitate testing of new inhibitors in an animal model with similarity to human ASM/MCL, we developed a murine model that is based on retro-orbital injection of P815 cells, a murine mastocytoma line expressing the homologous D814Y mutant of KIT, into syngeneic DBA/2 mice.
  • We found that the systemic disease induced by this approach is highly reproducible and resembles human ASM/MCL.
  • Malignant mast cells were consistently detected in the peripheral blood by morphology and fluorescence-activated cell sorting after a stable latency whose length could be modulated by inoculum size.
  • This easy and inexpensive tumor model should be useful for testing potential drugs with activity against KIT(D816V).
  • [MeSH-major] Disease Models, Animal. Leukemia, Mast-Cell / pathology. Mastocytosis / pathology
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Flow Cytometry. Immunophenotyping. Mice. Mice, Inbred DBA

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  • (PMID = 16543062.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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59. Malone EK, Rassnick KM, Wakshlag JJ, Russell DS, Al-Sarraf R, Ruslander DM, Johnson CS, Trump DL: Calcitriol (1,25-dihydroxycholecalciferol) enhances mast cell tumour chemotherapy and receptor tyrosine kinase inhibitor activity in vitro and has single-agent activity against spontaneously occurring canine mast cell tumours. Vet Comp Oncol; 2010 Sep;8(3):209-20
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  • [Title] Calcitriol (1,25-dihydroxycholecalciferol) enhances mast cell tumour chemotherapy and receptor tyrosine kinase inhibitor activity in vitro and has single-agent activity against spontaneously occurring canine mast cell tumours.
  • In this study, we examine whether calcitriol increases chemotherapy or tyrosine kinase inhibitor in vitro cytotoxicity in canine mastocytoma C2 cells.
  • We also evaluate the in vivo effect of DN101, a highly concentrated oral formulation of calcitriol designed specifically for cancer therapy, as a single-agent therapy in dogs with mast cell tumours (MCTs).
  • [MeSH-major] Calcitriol / therapeutic use. Calcium Channel Agonists / therapeutic use. Dog Diseases / drug therapy. Mastocytoma / veterinary. Skin Neoplasms / veterinary
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Benzamides. Blotting, Western / veterinary. Cell Line, Tumor. Dogs. Dose-Response Relationship, Drug. Drug Synergism. Female. Imatinib Mesylate. Indoles / pharmacology. Lomustine / pharmacology. Male. Piperazines / pharmacology. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / pharmacology. Pyrroles / pharmacology. Receptors, Calcitriol / analysis. Treatment Outcome. Vinblastine / pharmacology

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  • (PMID = 20691028.001).
  • [ISSN] 1476-5829
  • [Journal-full-title] Veterinary and comparative oncology
  • [ISO-abbreviation] Vet Comp Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA067267; United States / NCI NIH HHS / CA / R01 CA095045
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Calcium Channel Agonists; 0 / Indoles; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Pyrroles; 0 / Receptors, Calcitriol; 24F9PF7J3R / toceranib phosphate; 5V9KLZ54CY / Vinblastine; 7BRF0Z81KG / Lomustine; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; FXC9231JVH / Calcitriol
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60. Heide R, Beishuizen A, De Groot H, Den Hollander JC, Van Doormaal JJ, De Monchy JG, Pasmans SG, Van Gysel D, Oranje AP, Dutch National Mastocytosis Work Group: Mastocytosis in children: a protocol for management. Pediatr Dermatol; 2008 Jul-Aug;25(4):493-500
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  • Mastocytosis is characterized by an increased number of mast cells with an abnormal growth and accumulation in one or more organs.
  • Generally, we recognize three more common forms of cutaneous mastocytosis: maculopapulous mastocytosis (formerly urticaria pigmentosa), mastocytoma of skin, and diffuse cutaneous mastocytosis.
  • In most cases of mastocytosis, only yearly checkups are necessary and no treatment is required; preventive recommendations are warranted in those individuals with systemic disease and constitutional symptoms.

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  • (PMID = 18789103.001).
  • [ISSN] 1525-1470
  • [Journal-full-title] Pediatric dermatology
  • [ISO-abbreviation] Pediatr Dermatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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61. Kiderlen AF, Tata PS, Ozel M, Laube U, Radam E, Schäfer H: Cytopathogenicity of Balamuthia mandrillaris, an opportunistic causative agent of granulomatous amebic encephalitis. J Eukaryot Microbiol; 2006 Nov-Dec;53(6):456-63
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  • The ameba is shown to lyse murine mastocytoma cells very efficiently in a time- and dose-related manner.
  • Furthermore, experiments involving semipermeable membranes and phagocytosis inhibitors indicate that the cytolytic activity of B. mandrillaris is essentially cell contact-dependent.

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  • (PMID = 17123409.001).
  • [ISSN] 1066-5234
  • [Journal-full-title] The Journal of eukaryotic microbiology
  • [ISO-abbreviation] J. Eukaryot. Microbiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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62. Yang HZ, Xu S, Liao XY, Zhang SD, Liang ZL, Liu BH, Bai JY, Jiang C, Ding J, Cheng GF, Liu G: A novel immunostimulator, N-[alpha-O-benzyl-N-(acetylmuramyl)-L-alanyl-D-isoglutaminyl]-N6-trans-(m-nitrocinnamoyl)-L-lysine, and its adjuvancy on the hepatitis B surface antigen. J Med Chem; 2005 Aug 11;48(16):5112-22
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  • The present study shows that MDP-C induces strong cytolytic activity by macrophages on P388 leukemia cells and cytotoxic activity by cytotoxic T lymphocytes (CTLs) on P815 mastocytoma cells.
  • Moreover, MDP-C remarkably enhances the immune system's responsiveness to hepatitis B surface antigen (HBsAg) in hepatitis B virus transgenic mice for both antibody production and specific HBsAg T-cell responses ex vivo.
  • [MeSH-minor] Animals. Antibody Formation. Antigens, CD11c / biosynthesis. Bone Marrow Cells / drug effects. Bone Marrow Cells / metabolism. Cell Line, Tumor. Cytotoxicity, Immunologic. Dendritic Cells / drug effects. Dendritic Cells / metabolism. Hepatitis B / immunology. Hepatitis B Vaccines / immunology. Histocompatibility Antigens Class I / biosynthesis. In Vitro Techniques. Intercellular Adhesion Molecule-1 / biosynthesis. Interleukin-12 / biosynthesis. Interleukin-2 / biosynthesis. Macrophages / drug effects. Macrophages / immunology. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Rabbits. Rats. Rats, Wistar. T-Lymphocytes, Cytotoxic / drug effects. T-Lymphocytes, Cytotoxic / immunology. Toxicity Tests, Acute

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  • (PMID = 16078831.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / U01 AI 61092-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antigens, CD11c; 0 / Hepatitis B Surface Antigens; 0 / Hepatitis B Vaccines; 0 / Histocompatibility Antigens Class I; 0 / Interleukin-2; 0 / N(2)-(O-benzyl-N-(acetylmuramyl)-alanyl-isoglutaminyl)-N(6)-(3-nitrocinnamoyl)-lysine; 126547-89-5 / Intercellular Adhesion Molecule-1; 187348-17-0 / Interleukin-12; 53678-77-6 / Acetylmuramyl-Alanyl-Isoglutamine
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63. Shi G, Mao J, Yu G, Zhang J, Wu J: Tumor vaccine based on cell surface expression of DcR3/TR6. J Immunol; 2005 Apr 15;174(8):4727-35
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  • [Title] Tumor vaccine based on cell surface expression of DcR3/TR6.
  • Solid-phase TR6 can trigger reverse signaling of LIGHT and FasL expressed on T cells, and lead to T cell costimulation.
  • In this study, we engineered tumor cells to express cell surface TR6 and used these cells as a tumor vaccine.
  • We demonstrated that mastocytoma P815 cells expressing surface TR6 (TR6-P815) effectively augmented the T cells response in vitro and ex vivo in terms of proliferation, as well as IL-2 and IFN-gamma secretion.
  • The cell surface TR6-based tumor vaccine was also effective against low antigenicity tumors, such as B16 melanoma; co-administration of bacillus Calmette-Guérin further enhanced the vaccine's efficacy.
  • Thus, cell surface TR6 expression is a useful addition to our tumor vaccine arsenal.
  • [MeSH-major] Cancer Vaccines / isolation & purification. Membrane Glycoproteins / immunology. Receptors, Cell Surface / immunology. Receptors, Tumor Necrosis Factor / immunology
  • [MeSH-minor] Animals. Antigens, Neoplasm. Cell Line, Tumor. Cell Membrane / immunology. Female. Humans. Immunologic Factors / administration & dosage. In Vitro Techniques. Lymphocyte Activation. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Mice, Knockout. Mice, Nude. Neoplasms, Experimental / immunology. Neoplasms, Experimental / therapy. Receptors, Tumor Necrosis Factor, Member 6b. T-Lymphocytes / immunology

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  • (PMID = 15814697.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Immunologic Factors; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Member 6b; 0 / TNFRSF6B protein, human
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64. Neub A, Krahl D, Stich A, Amon U: Cutaneous infection with Leishmania infantum in an infant treated successfully with miltefosine. J Dtsch Dermatol Ges; 2008 Dec;6(12):1061-4

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  • Various topical treatments at other hospitals for the working diagnosis of mastocytoma failed to prevent a slow increase in size and the onset of systemic signs and symptoms.

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  • (PMID = 18498377.001).
  • [ISSN] 1610-0387
  • [Journal-full-title] Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG
  • [ISO-abbreviation] J Dtsch Dermatol Ges
  • [Language] eng; ger
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antifungal Agents; 107-73-3 / Phosphorylcholine; 53EY29W7EC / miltefosine
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65. Duran-Struuck R, Tawara I, Lowler K, Clouthier SG, Weisiger E, Rogers C, Luker G, Kumanogoh A, Liu C, Ferrara JL, Reddy P: A novel role for the semaphorin Sema4D in the induction of allo-responses. Biol Blood Marrow Transplant; 2007 Nov;13(11):1294-1303
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  • We tested the requirement of Sema4D expression on T cells in the induction of T cell allo-immune responses.
  • Further studies demonstrated that the reduced proliferation was not due to intrinsic T cell defects, and that the cytotoxic functions were preserved.
  • After allo-geneic bone marrow transplant (BMT), recipients of Sema4D-/- T cells showed reduced mortality and graft-versus-host disease (GVHD) target organ damage.
  • When BALB/c recipient mice were challenged with the P815 murine mastocytoma cell line (H2(d)) the recipients of allo-geneic Sema4D-/- B6 T cells showed a significant improvement in tumor free survival when compared to syngeneic recipients, thus demonstrating preservation of GVL, albeit of a lesser magnitude than allo-geneic wt T cells.
  • In summary, Sema4D plays a significant role in mediating in vitro and in vivo allo-geneic responses by modulating T cell-APC interactions.

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  • (PMID = 17950916.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / T32 RR007008; United States / NIAID NIH HHS / AI / K08 AI052863; United States / NIAID NIH HHS / AI / K08 AI052863-04; United States / NCRR NIH HHS / RR / T32 RR07008-21A1; United States / NIAID NIH HHS / AI / AI052863-04; United States / NCI NIH HHS / CA / 5 P01 CA039542-20; United States / NCI NIH HHS / CA / P01 CA039542; United States / NIAID NIH HHS / AI / 5 K08 AI052863-04
  • [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 / Sema4d protein, mouse; 0 / Semaphorins
  • [Other-IDs] NLM/ NIHMS33785; NLM/ PMC2278022
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66. Gleixner KV, Rebuzzi L, Mayerhofer M, Gruze A, Hadzijusufovic E, Sonneck K, Vales A, Kneidinger M, Samorapoompichit P, Thaiwong T, Pickl WF, Yuzbasiyan-Gurkan V, Sillaber C, Willmann M, Valent P: Synergistic antiproliferative effects of KIT tyrosine kinase inhibitors on neoplastic canine mast cells. Exp Hematol; 2007 Oct;35(10):1510-21
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  • [Title] Synergistic antiproliferative effects of KIT tyrosine kinase inhibitors on neoplastic canine mast cells.
  • Aggressive mast cell (MC) tumors are hematopoietic neoplasms characterized by uncontrolled growth of MC and resistance to conventional drugs.
  • In most cases, the tyrosine kinase (TK) receptor KIT is involved in malignant cell growth.
  • We examined the effects of four TK inhibitors (imatinib, midostaurin, nilotinib, and dasatinib) on C2 canine mastocytoma cells, as well as primary neoplastic canine MC.
  • Growth-inhibitory effects of TK inhibitors were also observed in primary neoplastic mast cells, although IC(50) values for each drug varied from patient to patient, with midostaurin being the most potent agent in all samples tested.
  • In flow cytometry and TUNEL assay experiments, growth-inhibitory effects of TK inhibitors were found to be associated with cell-cycle arrest and apoptosis.
  • Together, these data show that several TK-targeting drugs induce apoptosis and inhibit proliferation in canine mastocytoma cells in vitro, and that synergistic drug interactions can be obtained.
  • [MeSH-major] Dog Diseases / drug therapy. Hematologic Neoplasms / drug therapy. Hematologic Neoplasms / veterinary. Mast-Cell Sarcoma / drug therapy. Mast-Cell Sarcoma / veterinary. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-kit / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line, Tumor. Dogs. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm / drug effects. Drug Screening Assays, Antitumor. Drug Synergism. Humans. Mast Cells / metabolism. Mast Cells / pathology

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  • (PMID = 17681669.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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67. Conrad H, Gausche-Hill M, Burbulys D: A 6-month old with total body flushing and a macular-papular lesion. Pediatr Emerg Care; 2007 May;23(5):321-3
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  • A rare cause of this condition results in the release of mast cell mediators such as histamine, prostaglandin D2, tryptase, chymase, and leukotrienes.
  • We present a case of a 6-month-old with severe total body flushing and a yellow-tan, raised, well-demarcated lesion on the thigh consistent with a solitary mastocytoma.
  • [MeSH-major] Flushing / etiology. Mastocytoma / diagnosis

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  • (PMID = 17505276.001).
  • [ISSN] 1535-1815
  • [Journal-full-title] Pediatric emergency care
  • [ISO-abbreviation] Pediatr Emerg Care
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histamine H1 Antagonists; 8GTS82S83M / Diphenhydramine
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68. Fawcett H, Mader JS, Robichaud M, Giacomantonio C, Hoskin DW: Contribution of reactive oxygen species and caspase-3 to apoptosis and attenuated ICAM-1 expression by paclitaxel-treated MDA-MB-435 breast carcinoma cells. Int J Oncol; 2005 Dec;27(6):1717-26
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  • Furthermore, adhesion molecule expression is attenuated on mouse mastocytoma and human leukemia cells that survive short-term culture in the presence of paclitaxel.
  • [MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Caspase 3. Caspase Inhibitors. Cell Line, Tumor. Cell Survival / drug effects. Cysteine Proteinase Inhibitors / pharmacology. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Fibronectins / metabolism. Humans. Intracellular Membranes / drug effects. Intracellular Membranes / physiology. Membrane Potentials / drug effects. Mitochondria / drug effects. Mitochondria / physiology. Oligopeptides / pharmacology. Time Factors

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  • (PMID = 16273228.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Antineoplastic Agents, Phytogenic; 0 / Caspase Inhibitors; 0 / Cysteine Proteinase Inhibitors; 0 / Fibronectins; 0 / Oligopeptides; 0 / Reactive Oxygen Species; 0 / benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 126547-89-5 / Intercellular Adhesion Molecule-1; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; P88XT4IS4D / Paclitaxel
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69. Liu Z, Garrard WT: Long-range interactions between three transcriptional enhancers, active Vkappa gene promoters, and a 3' boundary sequence spanning 46 kilobases. Mol Cell Biol; 2005 Apr;25(8):3220-31
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Very similar interactions between the enhancers are also exhibited by normal B cells isolated from mouse splenic tissue but not by germ line transcriptionally inactive alleles of T cells or P815 mastocytoma cells, which exhibit a seemingly linear chromatin organization.

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  • (PMID = 15798207.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM029935; United States / NIGMS NIH HHS / GM / R01 GM059809; United States / NIGMS NIH HHS / GM / GM29935; United States / NIGMS NIH HHS / GM / GM59809
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin; 0 / DNA-Binding Proteins; 0 / Immunoglobulin Variable Region; 0 / Immunoglobulin kappa-Chains; 0 / NF-kappa B; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; 0 / Transcription Factor RelA; 0 / Transcription Factors; 9004-22-2 / Globins; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC1069589
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70. Wang L, Liu JQ, Talebian F, El-Omrani HY, Khattabi M, Yu L, Bai XF: Tumor expression of CD200 inhibits IL-10 production by tumor-associated myeloid cells and prevents tumor immune evasion of CTL therapy. Eur J Immunol; 2010 Sep;40(9):2569-79

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor expression of CD200 inhibits IL-10 production by tumor-associated myeloid cells and prevents tumor immune evasion of CTL therapy.
  • CD200 is a cell-surface glycoprotein that functions through interaction with the CD200 receptor on myeloid lineage cells to regulate myeloid cell functions.
  • Expression of CD200 has been implicated in multiple types of human cancer; however, the impact of tumor expression of CD200 on tumor immunity remains poorly understood.
  • To evaluate this issue, we generated CD200-positive mouse plasmacytoma J558 and mastocytoma P815 cells.
  • We found that established CD200-positive tumors were often completely rejected by adoptively transferred CTL without tumor recurrence; in contrast, CD200-negative tumors were initially rejected by adoptively transferred CTL but the majority of tumors recurred.
  • Tumor expression of CD200 significantly inhibited suppressive activity and IL-10 production by tumor-associated myeloid cells (TAMC), and as a result, more CTL accumulated in the tumor and exhibited a greater capacity to produce IFN-gamma in CD200-positive tumors than in CD200-negative tumors.
  • Neutralization of IL-10 significantly inhibited the suppressor activity of TAMC, and IL-10-deficiency allowed TAMC to kill cancer cells and their antigenic variants, which prevented tumor recurrence during CTL therapy.
  • Thus, tumor expression of CD200 prevents tumor recurrence via inhibiting IL-10 production by TAMC.

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  • (PMID = 20662098.001).
  • [ISSN] 1521-4141
  • [Journal-full-title] European journal of immunology
  • [ISO-abbreviation] Eur. J. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA138427-03; United States / NCI NIH HHS / CA / R01 CA138427; United States / NCI NIH HHS / CA / R01 CA138427-03; United States / NCI NIH HHS / CA / R01CA138427
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / antigens, CD200; 130068-27-8 / Interleukin-10
  • [Other-IDs] NLM/ NIHMS257438; NLM/ PMC3003298
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71. Shanker A, Verdeil G, Buferne M, Inderberg-Suso EM, Puthier D, Joly F, Nguyen C, Leserman L, Auphan-Anezin N, Schmitt-Verhulst AM: CD8 T cell help for innate antitumor immunity. J Immunol; 2007 Nov 15;179(10):6651-62

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD8 T cell help for innate antitumor immunity.
  • We demonstrate that monoclonal CD8 T lymphocytes reactive to tumor Ag P1A on P815 mastocytoma cells provide essential "help" to NK cells for rejection of P1A-deficient tumors.
  • RAG-deficient mice have normal NK cells but do not reject either tumor.
  • Reconstitution of these mice with P1A-specific T cells conferred resistance to both P1A-expressing and -deficient tumor cells provided they were present at the same site.
  • Elimination of Ag-negative tumor variants required both activated T and NK cells.
  • However, CD8 T cell help to NK cells appeared ineffective for P1A-negative variants separated from the P1A-positive tumor.
  • Local tumor Ag-specific T cell-NK cell collaboration results in the elimination of tumor cells whether they express or not the T cell tumor Ag epitope, thus containing the emergence of tumor escape variants before metastasis.
  • [MeSH-major] Antigens, Neoplasm / immunology. CD8-Positive T-Lymphocytes / immunology. Homeodomain Proteins / immunology. Immunity, Innate. Killer Cells, Natural / immunology. Mast-Cell Sarcoma / immunology
  • [MeSH-minor] Animals. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / immunology. Graft Rejection / genetics. Graft Rejection / immunology. Lymphocyte Activation / immunology. Mice. Mice, Mutant Strains. Neoplasm Transplantation. Oligonucleotide Array Sequence Analysis. Tumor Escape / immunology

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  • (PMID = 17982055.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Homeodomain Proteins; 0 / cancer-testis antigen P1A, mouse; 0 / tumor rejection antigen P815A, mouse; 128559-51-3 / RAG-1 protein
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72. Horiyama S, Honda C, Suwa K, Umemoto Y, Okada Y, Semma M, Ichikawa A, Takayama M: Sensitive and simple analysis of sorbic acid using liquid chromatography with electrospray ionization tandem mass spectrometry. Chem Pharm Bull (Tokyo); 2008 Apr;56(4):578-81
Hazardous Substances Data Bank. AMMONIUM ACETATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We also show that the method is useful to analyze SA level in the cytosol of mastocytoma cells, which were pretreated with SA.
  • [MeSH-minor] Acetates. Cell Differentiation. Cell Line, Tumor. Chromatography, Liquid. Cytosol / chemistry. Humans. Reproducibility of Results. Solvents. Spectrometry, Mass, Electrospray Ionization

  • Hazardous Substances Data Bank. SORBIC ACID .
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  • (PMID = 18379111.001).
  • [ISSN] 0009-2363
  • [Journal-full-title] Chemical & pharmaceutical bulletin
  • [ISO-abbreviation] Chem. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Acetates; 0 / Food Preservatives; 0 / Solvents; RRE756S6Q2 / ammonium acetate; X045WJ989B / Sorbic Acid
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73. Bouabdallah I, M'Barek LA, Zyad A, Ramdani A, Zidane I, Melhaoui A: Anticancer effect of three pyrazole derivatives. Nat Prod Res; 2006 Sep;20(11):1024-30
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The evaluation of the cytotoxic properties in vitro of three synthetic tripods containing pyrazole: N,N-bis[(3,5-dimethylpyrazol-1-yl)methyl]aniline (1); N,N-tetrakis[(3,5-dimethylpyrazol-1-yl)methyl]-para-phenylenediamine (2); and N,N-tetrakis-[(1,5-dimethylpyrazol-3-yl)methyl]-para-phenylenediamine (3), was examined for their cytotoxic activity on two tumor cell lines: P815 (murin mastocytoma) and Hep (human laryngeal carcinome).
  • While the compound 2 shows a small cytotoxic activity, compounds 1 and 3 are more cytotoxic against both cell lines.
  • However, this cytotoxicity is more pronounced against Hep cell line (IC50: 3.25 microg mL(-1) for compound 1 and 6.92 microg mL(-1) for compound 3) than P815 cell line (IC50: 17.82 microg mL(-1) for compound 1 and 37.21 microg mL(-1) for compound 3).
  • Interestingly, the cytotoxicity induced by compound 1 against Hep cell line is more important than that induced by adriamycin used as a positive control.
  • [MeSH-minor] Cell Line, Tumor. Humans. Molecular Structure

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  • (PMID = 17050185.001).
  • [ISSN] 1478-6419
  • [Journal-full-title] Natural product research
  • [ISO-abbreviation] Nat. Prod. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aniline Compounds; 0 / Antineoplastic Agents; 0 / N,N-bis((3,5-dimethylpyrazol-1-yl)methyl)aniline; 0 / N,N-tetrakis((3,5-dimethylpyrazol-1-yl)methyl)-para-phenylenediamine; 0 / Phenylenediamines; 0 / Pyrazoles
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74. Albrecht M, Müller K, Köhn FM, Meineke V, Mayerhofer A: Ionizing radiation induces degranulation of human mast cells and release of tryptase. Int J Radiat Biol; 2007 Aug;83(8):535-41
Hazardous Substances Data Bank. Cetirizine .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ionizing radiation induces degranulation of human mast cells and release of tryptase.
  • PURPOSE: Skin fibrosis is a hallmark of ionizing radiation-induced tissue injury and we hypothesized that mast cells via their products (especially tryptase) are involved in this event.
  • We therefore investigated whether: (i) irradiation with 5 Gray (Gy) is able to induce the release of the typical mast cell mediator tryptase from human mast cells (HMC-1) in vitro, (ii) this effect can be influenced by application of clinically relevant mast cell blockers, and (iii) irradiation leads to mast cell degranulation in ex vivo skin culture models.
  • MATERIALS AND METHODS: The human mast cell line (HMC)-1, as well as ex vivo skin tissue served as experimental models.
  • Fluorescence activated cell sorting (FACS), Enzyme linked immunosorbent assays (ELISA), mast cell degranulation assays and immunohistochemistry were applied.
  • Mast cell degranulation and secretion of tryptase was partially, but not significantly, inhibited by pre-incubation with the histamine-1 receptor (H1) blocker cetirizine.
  • Mast cell degranulation was also clearly evident after irradiation using an ex vivo skin culture model of mastocytoma tissue.
  • CONCLUSIONS: We propose that ionizing radiation leads to a degranulation of dermal mast cells, an event which is accompanied by the release of tryptase.
  • [MeSH-major] Cell Degranulation / radiation effects. Mast Cells / radiation effects. Mast-Cell Sarcoma / radionuclide imaging. Skin / radiation effects. Tryptases / radiation effects

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  • (PMID = 17613126.001).
  • [ISSN] 0955-3002
  • [Journal-full-title] International journal of radiation biology
  • [ISO-abbreviation] Int. J. Radiat. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histamine H1 Antagonists; EC 3.4.21.59 / Tryptases; YO7261ME24 / Cetirizine
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75. Ohno M, Kitabatake N, Tani F: Functional region of mouse heat shock protein 72 for its binding to lymphoid neoplastic P388D1 cells. Mol Immunol; 2007 Mar;44(9):2344-54
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In the present study, we examined which region of mouse Hsp72 interacted with this cell line by using truncated variants that are sequentially lacking sections of the C-terminal region.
  • The full-length mouse Hsp72 specifically bound to P388D1 cells, but not to mastocytoma P815 cells.
  • However, the variant lacking the substrate-binding domain did not show any binding to this cell line.

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
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  • (PMID = 17126904.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HSP72 Heat-Shock Proteins; 0 / Mutant Proteins; 0 / Recombinant Proteins
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76. Nishikawa H, Kitani S: Tea catechins have dual effect on mast cell degranulation induced by compound 48/80. Int Immunopharmacol; 2008 Sep;8(9):1207-15
Hazardous Substances Data Bank. HYDROGEN PEROXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tea catechins have dual effect on mast cell degranulation induced by compound 48/80.
  • We investigated catechin's effects on intracellular ROS generation in mast cell activation and degranulation.
  • Compound 48/80, receptor mimetic basic secretagogues for mast cell, induced ROS generation dose-dependently with bell-shaped degranulation pattern in canine cutaneous mastocytoma cells (CM-MC).
  • [MeSH-major] Antioxidants / pharmacology. Catechin / pharmacology. Cell Degranulation / drug effects. Mast Cells / drug effects. Tea / chemistry. p-Methoxy-N-methylphenethylamine / antagonists & inhibitors. p-Methoxy-N-methylphenethylamine / pharmacology

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • Hazardous Substances Data Bank. Green tea .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
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  • (PMID = 18602066.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Reactive Oxygen Species; 0 / Tea; 4091-50-3 / p-Methoxy-N-methylphenethylamine; 8R1V1STN48 / Catechin; BBX060AN9V / Hydrogen Peroxide; EC 2.7.10.1 / Protein-Tyrosine Kinases; SY7Q814VUP / Calcium
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77. Sakowski SA, Geddes TJ, Thomas DM, Levi E, Hatfield JS, Kuhn DM: Differential tissue distribution of tryptophan hydroxylase isoforms 1 and 2 as revealed with monospecific antibodies. Brain Res; 2006 Apr 26;1085(1):11-8
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • Analysis of mouse tissues confirms that TPH1 is the predominant form expressed in pineal gland and in P815 mastocytoma cells with a molecular weight of 51 kDa.
  • [MeSH-minor] Animals. Antibody Formation. Brain / enzymology. Cell Line, Tumor. Duodenum / enzymology. Gene Expression Regulation, Enzymologic / physiology. Immunoblotting / methods. Immunohistochemistry / methods. Immunoprecipitation / methods. Isoenzymes / metabolism. Mastocytoma. Mice. Mice, Inbred C57BL. Molecular Weight. Recombinant Proteins / immunology. Tissue Distribution

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  • (PMID = 16581041.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / DA014392; United States / NIDA NIH HHS / DA / DA10756; United States / NCRR NIH HHS / RR / RR00166; United States / NIDA NIH HHS / DA / T32 DA07310
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies; 0 / Isoenzymes; 0 / Recombinant Proteins; EC 1.14.16.4 / Tph1 protein, mouse; EC 1.14.16.4 / Tph2 protein, mouse; EC 1.14.16.4 / Tryptophan Hydroxylase
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78. Quetglas JI, Ruiz-Guillen M, Aranda A, Casales E, Bezunartea J, Smerdou C: Alphavirus vectors for cancer therapy. Virus Res; 2010 Nov;153(2):179-96
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  • Alphaviruses contain a single strand RNA genome that can be easily modified to express heterologous genes at very high levels in a broad variety of cells, including tumor cells.
  • Alphavirus vectors have been successfully used as vaccines to induce protective and therapeutic immune responses against many tumor-associated antigens in animal models of mastocytoma, melanoma, mammary, prostate, and virally induced tumors.
  • Alphavirus vectors have also shown a high antitumoral efficacy by expressing antitumoral molecules in tumor cells, which include cytokines, antiangiogenic factors or toxic proteins.
  • In these studies induction of apoptosis in tumor cells contributed to the antitumoral efficacy by the release of tumor antigens that can be uptaken by antigen presenting cells, enhancing immune responses against tumors.
  • The fact that this latter virus has a natural tropism for tumor cells has led to many studies in which this vector was able to reach metastatic tumors when administered systemically.
  • [MeSH-minor] Animals. Apoptosis. Female. Genetic Therapy / methods. Humans. Interferon Type I / immunology. Male. Mammary Neoplasms, Animal / therapy. Mastocytoma / therapy. Melanoma / therapy. Models, Animal. Oncolytic Viruses. Prostatic Neoplasms / therapy

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  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20692305.001).
  • [ISSN] 1872-7492
  • [Journal-full-title] Virus research
  • [ISO-abbreviation] Virus Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interferon Type I
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79. Roskoski R Jr: Signaling by Kit protein-tyrosine kinase--the stem cell factor receptor. Biochem Biophys Res Commun; 2005 Nov 11;337(1):1-13
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  • [Title] Signaling by Kit protein-tyrosine kinase--the stem cell factor receptor.
  • Signaling by stem cell factor and Kit, its receptor, plays important roles in gametogenesis, hematopoiesis, mast cell development and function, and melanogenesis.
  • Stem cell factor exists as both a soluble and a membrane-bound glycoprotein while Kit is a receptor protein-tyrosine kinase.
  • The complete absence of stem cell factor or Kit is lethal.
  • Deficiencies of either produce defects in red and white blood cell production, hypopigmentation, and sterility.
  • Gain-of-function mutations of Kit are associated with several human neoplasms including acute myelogenous leukemia, gastrointestinal stromal tumors, and mastocytomas.
  • Binding of stem cell factor to Kit results in receptor dimerization and activation of protein kinase activity.


80. Moulin D, Donzé O, Talabot-Ayer D, Mézin F, Palmer G, Gabay C: Interleukin (IL)-33 induces the release of pro-inflammatory mediators by mast cells. Cytokine; 2007 Dec;40(3):216-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin (IL)-33 induces the release of pro-inflammatory mediators by mast cells.
  • In this study, we demonstrate that IL-33 induces the production of pro-inflammatory mediators in mast cells.
  • IL-33 dose and time-dependently stimulated IL-6 secretion by P815 mastocytoma cells and primary mouse bone marrow-derived mast cells (BMMC).
  • These effects of IL-33 appeared to occur independently of mast cell degranulation, The results of this study show for the first time that IL-33, a novel member of the IL-1 family of cytokines, stimulates the production of pro-inflammatory mediators by mast cells in addition to its effect on T helper 2 responses.
  • [MeSH-major] Inflammation Mediators / immunology. Interleukins / pharmacology. Mast Cells / immunology
  • [MeSH-minor] Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / immunology. Bone Marrow Cells / metabolism. Cell Line. Chemokine CCL2 / biosynthesis. Chemokine CCL2 / immunology. Dose-Response Relationship, Drug. Inflammation / drug therapy. Inflammation / immunology. Inflammation / metabolism. Interleukin-1beta / biosynthesis. Interleukin-1beta / immunology. Interleukin-33. Membrane Proteins / immunology. Membrane Proteins / metabolism. Mice. Prostaglandin D2 / biosynthesis. Prostaglandin D2 / immunology. Protein Binding / immunology. Receptors, Interleukin. Th2 Cells / cytology. Th2 Cells / immunology. Time Factors. Tumor Necrosis Factor-alpha / biosynthesis. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 18023358.001).
  • [ISSN] 1096-0023
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ccl2 protein, mouse; 0 / Chemokine CCL2; 0 / Il1rl1 protein, mouse; 0 / Il33 protein, mouse; 0 / Inflammation Mediators; 0 / Interleukin-1beta; 0 / Interleukin-33; 0 / Interleukins; 0 / Membrane Proteins; 0 / Receptors, Interleukin; 0 / Tumor Necrosis Factor-alpha; RXY07S6CZ2 / Prostaglandin D2
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81. Tani F, Nishikawa S, Yokoyama I, Hashimoto K, Nakamoto M, Nomura M, Tao Y, Kitabatake N: Lymphoid neoplastic P388D1 cells express membrane protein candidates that discriminate among the C-terminal phylogenetic diversity in heat shock protein 70 sequences. Mol Immunol; 2010 Nov-Dec;48(1-3):191-202

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  • Recombinant mouse inducible-type Hsp72 bound extensively to P388D1 cells in a saturable manner, but not to P815 mastocytoma or EL4 thymoma.
  • Analyses of surface antigens showed that B220, and CD19, but not CD91, LOX-1, and CD40, the HSP70 receptors reported so far, were present on P388D1 cells, suggesting a B-cell lineage for this cell line.
  • The binding of HSP70 to P388D1 cells was partially, but significantly, antagonized by fucoidan and maleylated BSA, implying a few types of scavenger receptors to be responsible for the binding of HSP70 to this cell line.
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line, Tumor / immunology. Cell Line, Tumor / metabolism. Cell Separation. Escherichia coli / genetics. Escherichia coli / immunology. Escherichia coli / metabolism. Flow Cytometry. Lactobacillus acidophilus / genetics. Lactobacillus acidophilus / immunology. Lactobacillus acidophilus / metabolism. Mice. Molecular Sequence Data. Phylogeny. Protein Binding. Sequence Alignment. Sequence Analysis, Protein. Species Specificity. Spinacia oleracea / genetics. Spinacia oleracea / immunology. Spinacia oleracea / metabolism

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20880591.001).
  • [ISSN] 1872-9142
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HSP70 Heat-Shock Proteins
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82. Xu P, Okkeri J, Hanisch S, Hu RY, Xu Q, Pomorski TG, Ding XY: Identification of a novel mouse P4-ATPase family member highly expressed during spermatogenesis. J Cell Sci; 2009 Aug 15;122(Pt 16):2866-76
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  • Furthermore, loss-of-function of FetA by RNA interference in mastocytoma P815 cells profoundly perturbs the structural organization of the Golgi complex and causes loss of constitutive secretion at lower temperature.
  • [MeSH-minor] Amino Acid Sequence. Animals. Biological Transport. Cell Line, Tumor. Endocytosis. Gene Deletion. Gene Expression Profiling. Gene Expression Regulation, Developmental. Golgi Apparatus / enzymology. Golgi Apparatus / pathology. Golgi Apparatus / ultrastructure. Lipid Metabolism. Male. Mastocytoma / enzymology. Mastocytoma / pathology. Mice. Molecular Sequence Data. Organ Specificity. Phylogeny. RNA, Messenger / genetics. RNA, Messenger / metabolism. Saccharomyces cerevisiae / metabolism. Sequence Alignment. Testis / cytology. Testis / embryology. Testis / enzymology


83. Sundram UN, Natkunam Y: Mast cell tryptase and microphthalmia transcription factor effectively discriminate cutaneous mast cell disease from myeloid leukemia cutis. J Cutan Pathol; 2007 Apr;34(4):289-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mast cell tryptase and microphthalmia transcription factor effectively discriminate cutaneous mast cell disease from myeloid leukemia cutis.
  • BACKGROUND: Cutaneous mast cell disorders are uncommon, but a subset, especially mastocytoma and mast cell leukemia, can histologically mimic myeloid leukemia cutis.
  • METHODS: We stained 17 cases of cutaneous mast cell disease and 20 cases of myeloid leukemia cutis with Giemsa, toluidine blue, or pinacyanol erythrosinate (PE), as well as with antibodies against mast cell tryptase, microphthalmia transcription factor (MiTF), CD117 (c-kit), myeloperoxidase, CD43, CD25, CD2, and CD68.
  • RESULTS: Mast cell tryptase and MiTF emerged as highly sensitive and specific markers for mast cell disease in this context, as both antibodies stained all cases of mast cell diseases but none of myeloid leukemia cutis.
  • Although CD117 stained all cases of mast cell disease, it also stained 2 of 18 cases of myeloid leukemia cutis.
  • PE appeared to be specific for mast cell disease, as 11 of 12 cases stained with this marker, compared with 0 of 18 cases of myeloid leukemia cutis.
  • CONCLUSIONS: Our results show that mast cell tryptase and MiTF are equally effective in distinguishing mast cell disease from myeloid leukemia cutis.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Mast Cells / pathology. Mastocytosis, Cutaneous / diagnosis. Microphthalmia-Associated Transcription Factor / metabolism. Tryptases / metabolism

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  • (PMID = 17381798.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD2; 0 / Antigens, CD43; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Microphthalmia-Associated Transcription Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.21.59 / Tryptases
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84. Tan AS, Berridge MV: Differential effects of redox-cycling and arylating quinones on trans-plasma membrane electron transport. Biofactors; 2008;34(3):183-90
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  • For redox-cycling quinones, cell injury is associated with mitochondrial permeability transition, whereas arylating quinones directly depolarise the mitochondrial membrane and deplete ATP.
  • Here we investigate the effects of redox-cycling 2,3-dimethoxy-1,4-naphthoquinone (DMNQ), arylating 1,4-benzoquinone (BQ) and mixed mechanism 2-methyl-1,4-naphthoquinone (MNQ) on PMET, viability and growth of P815 mouse mastocytoma cells.BQ and MNQ rapidly and extensively inhibited PMET as determined by WST-1 /mPMS reduction (IC50 3.5-5 microM at 30 min) whereas the effects of DMNQ were less pronounced.
  • In contrast, MTT reduction (cytosolic NADH dehydrogenase activity over 30 min) was weakly inhibited by BQ (IC50 20 microM) but not by MNQ or DMNQ and cell viability was unaffected.
  • Treatment with DMNQ, MNQ and to a lesser extent BQ inhibited cell proliferation as determined by MTT reduction at 48 h.
  • [MeSH-major] Cell Membrane / drug effects. Cell Membrane / metabolism. Electron Transport / drug effects. Quinones / pharmacology
  • [MeSH-minor] Animals. Benzoquinones / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. Mice. Naphthoquinones / pharmacology. Oxidation-Reduction. Vitamin K 3 / pharmacology

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  • (PMID = 19734119.001).
  • [ISSN] 1872-8081
  • [Journal-full-title] BioFactors (Oxford, England)
  • [ISO-abbreviation] Biofactors
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / Naphthoquinones; 0 / Quinones; 3T006GV98U / benzoquinone; 6956-96-3 / 2,3-dimethoxy-1,4-naphthoquinone; 723JX6CXY5 / Vitamin K 3
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85. Reiter E, Azzi A, Zingg JM: Enhanced anti-proliferative effects of combinatorial treatment of delta-tocopherol and resveratrol in human HMC-1 cells. Biofactors; 2007;30(2):67-77
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  • Here we wanted to determine whether the combined treatment of mast cells with the two compounds inhibits cell proliferation more efficiently when compared to individual treatments.
  • Both compounds inhibit HMC-1 mastocytoma cell proliferation and reduce the activity of Protein Kinase B (PKB/Akt) by inhibiting its Ser473-phosphorylation.
  • Our data suggest that delta-tocopherol and resveratrol can act additively in reducing cell proliferation and PKB phosphorylation.
  • The combination of phytochemicals with relatively broad specificity on enzymes involved in signal transduction and gene expression may increase their activity in disease prevention by modulating several different molecular targets.
  • [MeSH-major] Cell Division / drug effects. Stilbenes / pharmacology. Tocopherols / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Drug Interactions. Enzyme Inhibitors / pharmacology. Humans. Mast Cells / drug effects. Mastocytoma. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. alpha-Tocopherol / pharmacology. beta-Tocopherol / pharmacology. gamma-Tocopherol / pharmacology

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  • (PMID = 18356579.001).
  • [ISSN] 0951-6433
  • [Journal-full-title] BioFactors (Oxford, England)
  • [ISO-abbreviation] Biofactors
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Stilbenes; 1406-66-2 / Tocopherols; 8EF1Z1238F / gamma-Tocopherol; 9U6A490501 / beta-Tocopherol; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; H4N855PNZ1 / alpha-Tocopherol; JU84X1II0N / delta-tocopherol; Q369O8926L / resveratrol
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86. Liu Y, Furuta K, Teshima R, Shirata N, Sugimoto Y, Ichikawa A, Tanaka S: Critical role of protein kinase C betaII in activation of mast cells by monomeric IgE. J Biol Chem; 2005 Nov 25;280(47):38976-81
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  • [Title] Critical role of protein kinase C betaII in activation of mast cells by monomeric IgE.
  • Accumulating evidence suggests that IgE-mediated activation of mast cells occurs even in the absence of antigen, which is referred to as "monomeric IgE" responses.
  • Although monomeric IgE was found to induce a wide variety of responses, such as up-regulation of the FcepsilonRI, survival, cytokine production, histamine synthesis, and adhesion to fibronectin, it remains to be clarified how mast cells are activated in the absence of antigen.
  • Monomeric IgE-induced Ca(2+) influx was not observed in a mouse mastocytoma cell line, which lacks the expression of PKCbetaII, although Ca(2+) influx induced by cross-linking of the FcepsilonRI was intact.
  • Transfection of PKCbetaII cDNA was found to restore the Ca(2+) influx induced by monomeric IgE in this cell line.
  • Furthermore, the dominant negative form of PKCbetaII (PKCbetaII/T500V) significantly suppressed the Ca(2+) influx, histamine synthesis, and interleukin-6 production in another mouse mast cell line, which is highly sensitive to monomeric IgE.
  • [MeSH-major] Immunoglobulin E / metabolism. Mast Cells / enzymology. Mast Cells / immunology. Protein Kinase C / metabolism
  • [MeSH-minor] Animals. Base Sequence. Calcium Signaling. Cell Line. DNA, Complementary / genetics. Histamine / biosynthesis. Interleukin-6 / biosynthesis. Mice. Protein Kinase C beta. RNA Interference. Receptors, IgE / metabolism. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Transfection

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  • (PMID = 16183638.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Interleukin-6; 0 / Receptors, IgE; 0 / Recombinant Proteins; 37341-29-0 / Immunoglobulin E; 820484N8I3 / Histamine; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C beta
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87. Welker P, Wanner R, Zuberbier T, Groneberg DA, Henz BM: Gene expression and regulation of transcription factor activator protein-2 alpha in human mast cells. Allergy; 2005 Aug;60(8):1046-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression and regulation of transcription factor activator protein-2 alpha in human mast cells.
  • BACKGROUND: The transcription factor activator protein (AP)-2 regulates cell-type specific gene expression during development and differentiation, but its role in mast cell development has so far not been explored.
  • METHODS: Gene expression and regulation of AP2 was assessed in normal skin, diseases with increased mast cell numbers, and in vitro models of mast cell differentiation.
  • RESULTS: AP-2alpha-protein was not detectable in normal skin but in mastocytoma lesional mast cells.
  • AP-2alpha-mRNA and -protein were also detected in leukemic mast cells (HMC-1), in the adherent fraction of peripheral blood (PBMC) and umbilical cord blood mononuclear cells (CBMC), and AP-2alpha-mRNA at low levels in isolated-purified mast cells.
  • In contrast, tryptase expression increased in all cells throughout culture, as did c-Kit in normal cells, whereas in both leukemic cell lines, c-Kit was maintained unchanged at about the same level.
  • CONCLUSIONS: These findings suggest a continuous activation of AP-2alpha in mastocytomas and mast cell leukemia and its transient upregulation during c-Kit dependent early steps of normal mast cell differentiation.
  • [MeSH-major] Gene Expression. Gene Expression Regulation. Mast Cells / metabolism
  • [MeSH-minor] Cell Aging / physiology. Cell Line. Fluorescent Antibody Technique. Humans. Immunohistochemistry. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Serine Endopeptidases / genetics. Serine Endopeptidases / metabolism. Skin / metabolism. Stem Cells / metabolism. Tryptases

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  • (PMID = 15969686.001).
  • [ISSN] 0105-4538
  • [Journal-full-title] Allergy
  • [ISO-abbreviation] Allergy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.59 / Tryptases
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88. Ghochikyan A, Mkrtichyan M, Loukinov D, Mamikonyan G, Pack SD, Movsesyan N, Ichim TE, Cribbs DH, Lobanenkov VV, Agadjanyan MG: Elicitation of T cell responses to histologically unrelated tumors by immunization with the novel cancer-testis antigen, brother of the regulator of imprinted sites. J Immunol; 2007 Jan 1;178(1):566-73
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  • [Title] Elicitation of T cell responses to histologically unrelated tumors by immunization with the novel cancer-testis antigen, brother of the regulator of imprinted sites.
  • Both DNA- and protein-based vaccines induced Ag-specific CD4(+) T cell proliferation with Th1 and Th2 cytokine profiles, respectively.
  • These cytolytic responses were observed across a wide range of different mouse cancers including mammary adenocarcinoma, glioma, leukemia, and mastocytoma.

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  • (PMID = 17182597.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI044809-06; United States / NIAID NIH HHS / AI / R01 AI044809; United States / NIAID NIH HHS / AI / R01 AI044809-06; United States / NIA NIH HHS / AG / AG020241-06; United States / NIAID NIH HHS / AI / R01 AI-44809; United States / NINDS NIH HHS / NS / R01 NS050895; United States / NINDS NIH HHS / NS / NS050895-04; United States / NIA NIH HHS / AG / R01 AG020241; United States / NIA NIH HHS / AG / R01 AG-20241; United States / NIA NIH HHS / AG / R01 AG020241-06; United States / NINDS NIH HHS / NS / R01 NS-050895; United States / NINDS NIH HHS / NS / R01 NS050895-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antigens, CD4; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Ctcfl protein, mouse; 0 / DNA-Binding Proteins; 0 / Histocompatibility Antigens Class I; 0 / Interleukin-18; 0 / Vaccines, DNA; 187348-17-0 / Interleukin-12
  • [Other-IDs] NLM/ NIHMS47187; NLM/ PMC2377412
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89. Satake A, Inoue T, Kubo S, Taniguchi Y, Imado T, Fujioka T, Horiuchi M, Xu Y, Ikegame K, Yoshihara S, Kaida K, Tamaki H, Okada M, Okamura H, Ogawa H: Separation of antileukemic effects from graft-versus-host disease in MHC-haploidentical murine bone marrow transplantation: participation of host immune cells. Int J Hematol; 2010 Apr;91(3):485-97
MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Separation of antileukemic effects from graft-versus-host disease in MHC-haploidentical murine bone marrow transplantation: participation of host immune cells.
  • Allogeneic hematopoietic stem cell transplantation (HSCT) is associated with both graft-versus-host disease (GVHD) and graft-versus-leukemia (GVL) effects.
  • Recipient BDF1 (H-2(b/d)) mice received T cell-depleted bone marrow and spleen cells from B6C3F1 (H-2(b/k)) or C57BL/6 (H-2(b)) mice with or without P815 mastocytoma cells (H-2(d)) after receiving lethal total body irradiation.
  • [MeSH-major] Bone Marrow Transplantation / immunology. Graft vs Host Disease / immunology. Graft vs Host Disease / pathology. Graft vs Leukemia Effect / immunology. Major Histocompatibility Complex / immunology

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  • (PMID = 20300982.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cxcr3 protein, mouse; 0 / Receptors, CXCR3; 82115-62-6 / Interferon-gamma
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90. Nomi H, Tashiro-Yamaji J, Yamamoto Y, Miura-Takeda S, Miyoshi-Higashino M, Takahashi T, Azuma H, Ueda H, Katsuoka Y, Kubota T, Yoshida R: Acute rejection of allografted CTL-susceptible leukemia cells from perforin/Fas ligand double-deficient mice. J Immunol; 2007 Aug 15;179(4):2180-6
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  • In the case of CTL-susceptible targets (e.g., P815 mastocytoma cells and EL-4 or RLmale1 T lymphoma cells), however, it is assumed that the CTL is the effector cell responsible for allograft rejection and that perforin and Fas ligand (FasL) pathways are the killing mechanisms.
  • The peritoneal exudate cells from gld or normal mice showed T cell-, TCRalphabeta-, and perforin-dependent cytotoxic activity against the allograft, whereas the exudate cells from perforin(-/-) mice exhibited almost full cytotoxic activity in the presence of Fas-Fc.
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Cell Line, Tumor. Cell Nucleus / immunology. Enzyme Inhibitors / pharmacology. Leukemia / genetics. Leukemia / immunology. Macrophage-1 Antigen / genetics. Macrophage-1 Antigen / immunology. Mice. Mice, Inbred BALB C. Mice, Knockout. Neoplasm Transplantation / immunology. Nitric Oxide Synthase Type II / antagonists & inhibitors. Nitric Oxide Synthase Type II / immunology. Perforin. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, alpha-beta / immunology. Transplantation, Homologous. omega-N-Methylarginine / pharmacology

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  • (PMID = 17675477.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Fas Ligand Protein; 0 / Macrophage-1 Antigen; 0 / Membrane Glycoproteins; 0 / Pore Forming Cytotoxic Proteins; 0 / Receptors, Antigen, T-Cell, alpha-beta; 126465-35-8 / Perforin; 27JT06E6GR / omega-N-Methylarginine; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse
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91. Olver S, Groves P, Buttigieg K, Morris ES, Janas ML, Kelso A, Kienzle N: Tumor-derived interleukin-4 reduces tumor clearance and deviates the cytokine and granzyme profile of tumor-induced CD8+ T cells. Cancer Res; 2006 Jan 1;66(1):571-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor-derived interleukin-4 reduces tumor clearance and deviates the cytokine and granzyme profile of tumor-induced CD8+ T cells.
  • An interleukin (IL)-4-containing tumor environment is reported to be beneficial for immune clearance of tumor cells in vivo; however, the effect of IL-4 on the effector CD8+ T cells contributing to tumor clearance is not well defined.
  • We have used the immunogenic HLA-CW3-expressing P815 (P.CW3) mastocytoma and investigated whether IL-4 expression by the tumor affects tumor clearance and, if so, whether it alters the tumor-induced Vbeta10+ CD8+ T-cell response.
  • P.CW3 were stably transfected with IL-4 or the empty control vector, and independent cell lines were injected i.p. into syngeneic DBA/2 mice.
  • Surprisingly, mice that received IL-4-producing tumor cells showed delayed primary tumor clearance and were significantly more prone to develop secondary tumors compared with mice receiving control tumor cells.
  • Tumor clearance was dependent on CD8+ T cells.
  • The IL-4-secreting P.CW3 tumor cells led to markedly higher mRNA expression of IL-4 and granzyme A and B but no differences in IFN-gamma and IL-2 production, cell proliferation, or ex vivo CTL activity in primary Vbeta10+ CD8+ T cells when compared with the control tumor cells.
  • We concluded that tumor-derived IL-4 selectively changed the quality of the tumor-induced CD8+ T-cell response and resulted in unexpected negative effects on tumor clearance.
  • These data bring into question the delivery of IL-4 to the tumor environment for improving tumor immunotherapy.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Interleukin-4 / immunology. Mastocytoma / immunology
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Gene Expression. HLA-C Antigens / immunology. Mice. Mice, Inbred DBA. T-Lymphocytes, Cytotoxic / immunology. Transfection

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  • (PMID = 16397274.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA-C Antigens; 0 / HLA-C*03 antigen; 207137-56-2 / Interleukin-4
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92. Munitz A, Bachelet I, Fraenkel S, Katz G, Mandelboim O, Simon HU, Moretta L, Colonna M, Levi-Schaffer F: 2B4 (CD244) is expressed and functional on human eosinophils. J Immunol; 2005 Jan 1;174(1):110-8
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  • Moreover, activation of eosinophils via 2B4 induced eosinophil-mediated cytotoxicity toward two malignant cell lines, i.e., mouse mastocytoma P815 and EBV-infected 721.221 B cell lines.
  • The demonstration that human eosinophils express a functional 2B4 receptor indicates a broader role for these cells in health and disease.
  • [MeSH-minor] Animals. Antigens, CD58 / immunology. Antigens, CD58 / metabolism. Basophils / immunology. Basophils / metabolism. Blotting, Western. Cells, Cultured. Cytotoxicity Tests, Immunologic. Eosinophil Peroxidase / immunology. Eosinophil Peroxidase / metabolism. Flow Cytometry. Glycoproteins / immunology. Glycoproteins / metabolism. Humans. Immunoglobulins / immunology. Immunoglobulins / metabolism. Immunophenotyping. Immunoprecipitation. Interferon-gamma / immunology. Interferon-gamma / metabolism. Interleukin-4 / immunology. Interleukin-4 / metabolism. Neutrophils / immunology. Neutrophils / metabolism. Receptors, Cell Surface. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15611233.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD58; 0 / CD244 protein, human; 0 / CD48 antigen; 0 / CD84 protein, human; 0 / Glycoproteins; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / Receptors, Immunologic; 169535-43-7 / CD150 antigen; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma; EC 1.11.1.- / Eosinophil Peroxidase
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93. Ait M'barek L, Ait Mouse H, Jaâfari A, Aboufatima R, Benharref A, Kamal M, Bénard J, El Abbadi N, Bensalah M, Gamouh A, Chait A, Dalal A, Zyad A: Cytotoxic effect of essential oil of thyme (Thymus broussonettii) on the IGR-OV1 tumor cells resistant to chemotherapy. Braz J Med Biol Res; 2007 Nov;40(11):1537-44
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  • [Title] Cytotoxic effect of essential oil of thyme (Thymus broussonettii) on the IGR-OV1 tumor cells resistant to chemotherapy.
  • The anti-tumor effect of the Moroccan endemic thyme (Thymus broussonettii) essential oil (EOT) was investigated in vitro using the human ovarian adenocarcinoma IGR-OV1 parental cell line OV1/P and its chemoresistant counterparts OV1/adriamycin (OV1/ADR), OV1/vincristine (OV1/VCR), and OV1/cisplatin (OV1/CDDP).
  • All of these cell lines elicited various degrees of sensitivity to the cytotoxic effect of EOT.
  • Using the DBA-2/P815 (H2d) mouse model, tumors were developed by subcutaneous grafting of tumor fragments of similar size obtained from P815 (murin mastocytoma cell line) injected in donor mouse.
  • Interestingly, intra-tumoral injection of EOT significantly reduced solid tumor development.
  • Indeed, by the 30th day of repeated EOT treatment, the tumor volumes of the animals were 2.00 +/- 0.27, 1.35 +/- 0.20, and 0.85 +/- 0.18 cm(3) after injection with 10, 30, or 50 microL per 72 h (six times), respectively, as opposed to 3.88 +/- 0.50 cm(3) for the control animals.
  • These data indicate that the EOT which contains carvacrol as the major component has an important in vitro cytotoxic activity against tumor cells resistant to chemotherapy as well as a significant antitumor effect in mice.


94. Roskoski R Jr: Structure and regulation of Kit protein-tyrosine kinase--the stem cell factor receptor. Biochem Biophys Res Commun; 2005 Dec 23;338(3):1307-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structure and regulation of Kit protein-tyrosine kinase--the stem cell factor receptor.
  • Signaling by stem cell factor and Kit, its receptor, play important roles in gametogenesis, hematopoiesis, mast cell development and function, and melanogenesis.
  • Stem cell factor exists as both a soluble and a membrane-bound glycoprotein while Kit is a glycoprotein receptor protein-tyrosine kinase.
  • The complete absence of stem cell factor or Kit is lethal.
  • Gain-of-function mutations of Kit are associated with several human neoplasms including acute myelogenous leukemia, gastrointestinal stromal tumors, mastocytomas, and nasal T-cell lymphomas.
  • Binding of stem cell factor to Kit results in receptor dimerization and activation of protein kinase activity.

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  • (PMID = 16226710.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Number-of-references] 43
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95. Singh VP, Singh S, Narang KK, Bhattacharya D: Aluminium(III), chromium(III) and iron(III) complexes with 5-iodouracil and 5-iodouracil-histidine and their antitumour activity. J Enzyme Inhib Med Chem; 2009 Feb;24(1):105-10
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  • In vivo antitumour effect of 5-iodouracil and its complexes was examined on C(3)H /He mice against P815 murine mastocytoma.
  • [MeSH-minor] Aluminum. Animals. Chromium. Histidine. Iron. Mastocytoma. Mice. Mice, Inbred Strains

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  • (PMID = 18618327.001).
  • [ISSN] 1475-6374
  • [Journal-full-title] Journal of enzyme inhibition and medicinal chemistry
  • [ISO-abbreviation] J Enzyme Inhib Med Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Metals, Heavy; 0 / iodouracil; 0R0008Q3JB / Chromium; 4QD397987E / Histidine; 56HH86ZVCT / Uracil; 63231-63-0 / RNA; 9007-49-2 / DNA; CPD4NFA903 / Aluminum; E1UOL152H7 / Iron
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96. Hao S, Bi X, Su L, Dong W, Moyana T, Xiang J: Molecular and immunophenotypical characterization of progressive and regressive leukemia cell lines. Cancer Biother Radiopharm; 2005 Jun;20(3):290-9
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  • [Title] Molecular and immunophenotypical characterization of progressive and regressive leukemia cell lines.
  • The P815 and P198 cell lines are clonally related mouse mastocytoma cell lines.
  • They differ in their biologic behavior in that P815 is a progressive tumor cell line, whereas P198 is a regressive one.
  • These cell lines have been extensively used as models for the study of tumor-host relationships and tumor immunology.
  • Although some of their biological properties have been well documented, the molecular mechanisms underlying tumor progression or regression have not been completely elucidated.
  • In this study, we characterized the growth behavior and immunophenotype of these two cell lines, and analyzed their gene profiles using a complementary deoxynucleic acid (cDNA) microarray composed of 514 immunologically relevant genes.
  • Our data showed that the two cell lines exhibited quite dissimilar and contrasting growth characteristics when inoculated into syngeneic mice.
  • From a molecular viewpoint, P815 cells showed a higher expression of genes promoting tumor growth, such as IGF-1, IL-8R, FGFR1, VEGF-A, and VEGF-B.
  • On the other hand, P198 tumor cells expressed CD11b and CD80, which favor the recruitment of lymphocytes and antigen-presenting cells (APCs), as well as the elicitation of antitumor immunity.
  • P198 tumor cells also depicted a higher expression of genes inhibiting tumor growth, such as TNF-alpha, SOCS-1, CIS1, 4-1BB, and GDF-10.
  • In conclusion, our results contribute further information in the understanding of the molecular mechanisms associated with the regression and progression of P815 and P198 tumor cells.
  • [MeSH-minor] Animals. Cell Line, Tumor. Disease Progression. Down-Regulation / genetics. Gene Expression Profiling. Mice. Mice, Inbred DBA. Neoplasm Transplantation / pathology. Up-Regulation / genetics

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  • (PMID = 15989474.001).
  • [ISSN] 1084-9785
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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97. Mahadevan B, Luch A, Bravo CF, Atkin J, Steppan LB, Pereira C, Kerkvliet NI, Baird WM: Dibenzo[a,l]pyrene induced DNA adduct formation in lung tissue in vivo. Cancer Lett; 2005 Sep 8;227(1):25-32
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  • To date, dibenzo[a,l]pyrene (DBP) has been found to be the strongest tumor-initiating PAH ever tested in rodent skin and mammary tumor models.
  • Toxicity of DBP was revealed by a decrease in body and organ weight of mice while no apparent cell death was observed on P815 mastocytoma cells (allograft model) in vitro.
  • However, treatment of P815 cells in vitro with the ultimate carcinogenic metabolite of DBP, the fjord region (-)-anti-11,12-diol 13,14-epoxide [(-)-anti-DBPDE], resulted in the total loss of cell viability.
  • [MeSH-minor] Animals. Cell Line. Cell Survival / drug effects. DNA Damage. Female. Mice. Mice, Inbred C57BL. Mice, Inbred DBA

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  • (PMID = 16051029.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 28825; United States / NIEHS NIH HHS / ES / P30ES00210
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Benzopyrenes; 0 / DNA Adducts; 191-30-0 / dibenzo(a,l)pyrene
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98. Sakanaka M, Tanaka S, Sugimoto Y, Ichikawa A: Essential role of EP3 subtype in prostaglandin E2-induced adhesion of mouse cultured and peritoneal mast cells to the Arg-Gly-Asp-enriched matrix. Am J Physiol Cell Physiol; 2008 Nov;295(5):C1427-33
Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

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  • [Title] Essential role of EP3 subtype in prostaglandin E2-induced adhesion of mouse cultured and peritoneal mast cells to the Arg-Gly-Asp-enriched matrix.
  • Accumulating evidence has indicated that mast cells can modulate a wide variety of immune responses.
  • Migration and adhesion play a critical role in regulation of tissue mast cell function, in particular, under inflammatory conditions.
  • We previously demonstrated that prostaglandin (PG) E(2) stimulates adhesion of a mouse mastocytoma cell line, P-815, to the Arg-Gly-Asp (RGD)-enriched matrix through cooperation between two PGE(2) receptor subtypes: EP3 and EP4 (Hatae N, Kita A, Tanaka S, Sugimoto Y, Ichikawa A.
  • We here investigated PGE(2)-induced adhesion of IL-3-dependent bone marrow-derived cultured mast cells (BMMCs).
  • We then investigated PGE(2)-induced adhesion of peritoneal mast cells to the RGD-enriched matrix.
  • EP3 subtype was found to be the dominant PGE receptor that expresses in mouse peritoneal mast cells.
  • PGE(2) induced adhesion of the peritoneal mast cells of the Ptger3(+/+) mice, but not that of the Ptger3(-/-) mice.
  • In rat peritoneal mast cells, PGE(2) or an EP3 agonist stimulated both Ca(2+) mobilization and adhesion to the RGD-enriched matrix.
  • These results suggested that the EP3 subtype plays a pivotal role in PGE(2)-induced adhesion of murine mast cells to the RGD-enriched matrix through Ca(2+) mobilization.
  • [MeSH-major] Calcium Signaling. Cell Adhesion. Dinoprostone / metabolism. Mast Cells / metabolism. Oligopeptides / metabolism. Receptors, Prostaglandin E / metabolism

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  • (PMID = 18815228.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Estrenes; 0 / Interleukin-3; 0 / Oligopeptides; 0 / Phosphodiesterase Inhibitors; 0 / Ptger3 protein, mouse; 0 / Ptger3 protein, rat; 0 / Pyrrolidinones; 0 / Receptors, Prostaglandin E; 0 / Receptors, Prostaglandin E, EP3 Subtype; 112648-68-7 / 1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione; 99896-85-2 / arginyl-glycyl-aspartic acid; EC 2.4.2.31 / Pertussis Toxin; EC 3.1.4.- / Type C Phospholipases; K7Q1JQR04M / Dinoprostone; SY7Q814VUP / Calcium
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99. Shanker A, Buferne M, Schmitt-Verhulst AM: Cooperative action of CD8 T lymphocytes and natural killer cells controls tumour growth under conditions of restricted T-cell receptor diversity. Immunology; 2010 Jan;129(1):41-54
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  • [Title] Cooperative action of CD8 T lymphocytes and natural killer cells controls tumour growth under conditions of restricted T-cell receptor diversity.
  • In mice expressing a transgenic T-cell receptor (TCR; TCRP1A) of DBA/2 origin with reactivity towards a cancer-germline antigen P1A, the number of TCRP1A CD8+ T cells in lymphoid organs is lower in DBA/2 than in B10.D2 or B10.D2(x DBA/2)F1 mice.
  • This reduction results from haemopoietic cell autonomous differences in the differentiation of the major histocompatibility complex class I-restricted TCRP1A thymocytes controlled by DBA/2 versus B10.D2-encoded genes.
  • We report here that the lower number of TCRP1A CD8+ T cells in DBA/2 mice correlated with their poor resistance to P1A-expressing mastocytoma solid tumours.
  • Hence, in the absence of a polyclonal T-cell repertoire, precursor frequencies of natural killer cells and tumour-specific CTL affect tumour resistance.

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  • (PMID = 20050329.001).
  • [ISSN] 0019-2805
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / Receptors, Antigen, T-Cell; 0 / cancer-testis antigen P1A, mouse
  • [Other-IDs] NLM/ PMC2807485
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100. Duryee MJ, Klassen LW, Jones BL, Willis MS, Tuma DJ, Thiele GM: Increased immunogenicity to P815 cells modified with malondialdehyde and acetaldehyde. Int Immunopharmacol; 2008 Aug;8(8):1112-8
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  • Aldehyde modified proteins have been associated with the development and/or progression of alcoholic liver disease (ALD).
  • Previous studies have shown that malondialdehyde (MDA) and acetaldehyde (AA) synergistically form a unique adduct (MAA) with soluble proteins, which are capable of inducing cytokine release, T-cell proliferation, and antibody production.
  • The purpose of this study was to determine whether MAA adduction can elicit similar responses to cells using a well-defined tumor model.
  • The mouse mastocytoma P815 tumor cell line was modified with MAA (P815-MAA) or left unmodified (P815) and 10(6) irradiated cells were injected into DBA/2 mice once a week for 5 weeks.
  • Finally, in tumor survival studies the mean survival was 14.25 days in PBS treated mice; 15.75 days with P815 immunized mice and 18.25 days with P815-MAA immunized mice.
  • It is thought that these studies define a model system that will be useful in assessing antibody and potentially T-cell responses to cells that are modified by MAA.

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  • (PMID = 18550015.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / R01 AA010435-11; United States / NIAAA NIH HHS / AA / R37 AA007818; United States / NIAAA NIH HHS / AA / R37 AA007818-17; United States / NIAAA NIH HHS / AA / AA007818-17; United States / NIAAA NIH HHS / AA / R01 AA010435; United States / NIAAA NIH HHS / AA / AA010435-11
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 187348-17-0 / Interleukin-12; 4Y8F71G49Q / Malondialdehyde; GO1N1ZPR3B / Acetaldehyde
  • [Other-IDs] NLM/ NIHMS56834; NLM/ PMC2518647
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