Topic
Canine Mastocytoma
About: Canine Mastocytoma is a research topic. Over the lifetime, 59 publications have been published within this topic receiving 1417 citations.
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TL;DR: It is demonstrated that although c-kit derived from canine MCT did not contain the previously described activating point mutations, 5 of the 11 tumors analyzed possessed novel mutations consisting of tandem duplications involving exons 11 and 12, suggesting that these mutations may contribute to the development or progression of canine M CT.
230 citations
TL;DR: The results suggest that the cloned canine A3 AR is structurally and pharmacologically more similar to human than to rat A3AR, and although A2B receptors play a major role in the regulation of BR mast cell degranulation, multiple AR subtypes and G proteins may influence mast cell functions.
Abstract: We cloned and characterized the canine A3 adenosine receptor (AR) and examined AR-induced degranulation of the BR line of canine mastocytoma cells. Canine A3AR transcript is found predominantly in spleen, lung, liver, and testes and encodes a 314-amino acid heptahelical receptor.125I-N6-Aminobenzyladenosine binds to two affinity states of canine A3AR withKD values of 0.7 ± 0.1 and 16 ± 0.8 nm, reflecting G protein-coupled and -uncoupled receptors, respectively. Xanthine antagonists bind with similar affinities to human, canine, and rabbit receptors but with 80–400-fold lower affinities to rat A3AR. Although canine BR mastocytoma cells contain A1AR, A2BAR, and A3AR, degranulation seems to be mediated primarily by A2BARs stimulated by the nonselective agonist 5′-N-ethylcarboxamidoadenosine (NECA) but not by the A3-selective agonistN6-(3-iodobenzyl)adenosine-5′-N-methylcarboxamide. NECA-stimulated degranulation is not prevented by pertussis toxin and is blocked by enprofylline (Ki = 7 μm), an antiasthmatic xanthine with low affinity (Ki > 100 μm) for A1AR, A2AAR, and A3AR. NECA increases canine mastocytoma cell cAMP, Ca2+, and inositol trisphosphate levels; these responses are antagonized half-maximally by 7–15 μm enprofylline. The results suggest that (i) the cloned canine A3AR is structurally and pharmacologically more similar to human than to rat A3AR; (ii) the A2BAR, and not the A1AR or A3AR, is principally responsible for adenosine-mediated degranulation of canine BR mastocytoma cells; and (iii) the BR cell A2BAR couples to both Ca2+ mobilization and cAMP accumulation. Although A2B receptors play a major role in the regulation of BR mast cell degranulation, multiple AR subtypes and G proteins may influence mast cell functions.
199 citations
TL;DR: In this paper, a novel HSP90 inhibitor, STA-9090, was evaluated against wild-type (WT) and mutant Kit in canine bone marrow-derived cultured mast cells (BMCMCs) and fresh malignant mast cells.
100 citations
TL;DR: KIT can be used as a reliable immunohistochemical marker for canine mast cells and undifferentiated mast cell tumors and there is an inverse correlation between the degree of differentiation and the expression of KIT.
Abstract: c-kit protooncogene encodes a type III transmembrane receptor kinase, the stem cell factor receptor, or KIT. The ligand of the KIT. stem cell factor, is a cytokine that stimulates mast cell growth and differentiation. We have studied immunohistochemically KIT expression in 23 canine mast cell tumors (MCTs), 10 histiocytomas, 5 malignant melanomas, and in 2 cell lines derived from mast cells (HMC-1, human and C2, canine). As expected, KIT was detected both in the human mast cell leukemia cell line (HMC- ) and in the canine mastocytoma cell line C2. In normal canine skin, KIT expression was confined to mast cells. All canine MCTs expressed KIT, although the intensity of the staining reaction varied considerably among the 23 neoplasms. Grade III tumors showed the highest expression of KIT, whereas grade I tumors showed the lowest expression of KIT. Two patterns of KIT expression were detected in mast cells. In normal canine mast cells and in some neoplastic mast cells, KIT appeared mainly on the cell membrane. However, in many canine MCTs, KIT is accumulated in the cytoplasm, usually near the cell nucleus. The meaning of these two patterns is not clear. Expression of KIT could not be detected immunohistochemically in any of the other neoplasias investigated. According to our results, it can be concluded that most, if not all, canine MCT express KIT. Furthermore, there is an inverse correlation between the degree of differentiation and the expression of KIT. Moreover, according to our results, KIT can be used as a reliable immunohistochemical marker for canine mast cells and undifferentiated mast cell tumors.
82 citations
TL;DR: It is concluded that dog mastocytoma cells can be established in continuous culture, thus providing a system for studying mast cell biology, including growth and development.
Abstract: We have previously characterized dog mastocytoma cells propagated in nude mice. We have established two of these lines (C1 and C2) in continuous culture. Freshly disaggregated mastocytoma cells were cultured in Dulbecco's modified Eagle's medium (DME)-H16 mixed with 50% Ham's F12 and supplemented with histidine and 5% allergic dog serum (ADS). Cells were fed every 3 d and passaged weekly. Growth was assessed by cell count. Cell growth was best supported by culture in 5% ADS. C1 cells grow in suspension in ADS and have been passaged 55 times with a doubling time of 37.4 ± 18.7 h (mean ± 1 SD; n = 15). C2 cells adhere to tissue culture plastic in ADS and have been passaged 26 times with a doubling time of 49.3 ± 12.5 h (n = 13). Morphologic and functional characteristics are unchanged from those described in cells propagated in nude mice. Histamine content for C1 is 0.46 ± 0.18 pg/cell (n = 12) and 0.07 ± 0.04 pg/cell (n = 6) for C2. Both lines contain the neutral protease tryptase and C2 contains chymase. ...
69 citations