Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

23 melanomas having the thickness, according to Breslow, up to 1.5 mm and 12 benign melanocytic tumours are studied. Ultrastructural examination gives additional information for differentiating benign and malignant melanocytic tumours. It is necessary to take into consideration such signs as the number and qualitative properties of melanosomes and premelanosomes, structure of nuclear membrane, that of nucleoli, non-specific microfilaments and mast cell infiltration of the tumour stroma. Some ultrastructural difference between lentigo-melanoma and other histological tumour types are noted.
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PMID:[Ultrastructural features of benign and malignant lesions of a melanocytic nature]. 152 1

Previously we reported that the mAb AD1 recognized a heavily glycosylated 50- to 60-kDa protein (AD1 Ag) sterically close to the high-affinity IgE receptor on rat basophilic leukemia (RBL-2H3) cells. The N-terminal amino acid sequence of the AD1 Ag was nearly identical to that of human CD63 (melanoma-associated Ag ME491). In this study we cloned the cDNA of AD1 Ag from a rat basophilic leukemia 2H3 cDNA library. An open reading frame of 238 amino acids was identified that contained the N-terminal 43 amino acid sequence. No evidence of a signal peptide was found. However, four predominantly hydrophobic stretches of sequence were predicted to form membrane-spanning helices, and three putative N-glycosylation sites were identified. The AD1 Ag and CD63 were highly conserved between rat and human, suggesting that the sequence of this protein is important for its function. By immunostaining various rat tissues, the AD1 Ag was found localized to mast cells. However, it was located to lysosomes, secretory granules and the plasma membrane of RBL-2H3 cells and to lysosomes and plasma membrane of many other cultured cell lines. The AD1 Ag could be induced by placing cells in culture. Fibroblasts and hepatocytes freshly isolated from rat embryos stained very weakly for AD1 Ag; however, after 24 to 48 h in culture they were strongly positive. This increase in the expression of the AD1 Ag was accompanied by an increase in detectable RNA message. Therefore, AD1/ME491/CD63 Ag is a mast cell marker in tissue, but is also associated with other cells in culture.
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PMID:The rat mast cell antigen AD1 (homologue to human CD63 or melanoma antigen ME491) is expressed in other cells in culture. 163 75

In a controlled study, malignant murine P815 mastocytoma cells exposed in vitro to distilled and deionized water died as a result of progressive swelling, degranulation, and membrane rupture. A 90% mean cell death occurred when cells obtained directly from culture were exposed to deionized water for 2 minutes. Of 6 cryopreserved malignant murine cell lines, which included Cloudman S91 melanoma, CMT-93 rectum carcinoma, MMT-06052 mammary carcinoma, and S-180 Sarcoma, only P815 mastocytoma and YAC-1 lymphoma were significantly (P less than 0.05) affected by hypotonic shock; Cloudman S91 melanoma cells were the most resistant. Mastocytoma cells were selectively killed by hypotonic solution, and lymphoma cells were also killed by isotonic saline solution. Local mast cell tumor (MCT) recurrence and percentage survival were evaluated in 12 cats (21 MCT) and 54 dogs (85 MCT) subjected to surgery alone or local infiltration of deionized water as an adjunct to surgery. Of all 16 incompletely excised MCT in cats, there was no local recurrence following injection. Four mast cell tumors (2 cats) regressed after being injected in situ. In dogs with clinical stage-I MCT, local recurrence was detected in 50% (5/10), but with injection after incomplete excision, local MCT recurrence was significantly (P less than 0.05) less (6.6%, 1/15). Percentage recurrence was significantly (P less than 0.05) less and survival significantly greater when incompletely excised grade-II MCT were injected. Mean follow-up period after surgery in cats and dogs was 35 and 23.4 months, respectively.
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PMID:Mast cell tumor destruction by deionized water. 211 68

The prevalence and treatment of 255 eyelid tumors in 200 dogs was related to breed, age, sex, location, and tumor type. Treatment methods included cryosurgery and surgical excision. The mean age of all dogs with eyelid tumors was 9.6 years (+/- 0.2 SEM). Beagles, Siberian Huskies, and English Setters had a higher risk of tumor development, whereas the mixed-breed dogs had a lower risk. Sebaceous tarsal gland adenomas, benign melanomas, and papillomas were observed most often (88%). Malignant tumors (melanoma, adenocarcinoma, basal cell carcinoma, mast cell tumor, squamous cell carcinoma, hemangiosarcoma, and myoblastoma) comprised 8.2% of the tumors. Tumor recurrence rates between dogs treated with cryosurgery and those treated surgically were not significantly different (15.1% and 10.5%, respectively). The mean recurrence time after cryosurgery was 7.4 months (+/- 1.9 SEM), whereas it was 28.3 months (+/- 7.2 SEM) after surgical excision. Using either treatment, the long-term side effects were similar. The overall cosmetic appearance was observed to be better with cryosurgery.
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PMID:Prevalence and treatment of palpebral neoplasms in the dog: 200 cases (1975-1983). 379 87

The involvement of mast cells in anti-tumor resistance was studied by employing 2 strains of mast cell deficient but otherwise immunocompetent mice on a C57BL/6 (H-2b) background (W/Wv and Sl/Sld) and their respective normal +/+ littermate controls. Sensitization of control mice with irradiated semisyngeneic B16 melanoma cells (H-2b) resulted in protection against subsequent challenge with viable B16 cells, in contrast to sensitization of either W/Wv or Sl/Sld mice. The involvement of serotonin in antitumor resistance was studied by employing 2 serotonin active drugs: reserpine, that depletes mast cells of serotonin; and methysergide, a serotonin antagonist. Sensitization of BDF1 mice with irradiated B16 cells and sensitization of DBA/2 mice (H-2d) with irradiated SL2 cells (H-2d) resulted in protection against subsequent challenge with viable B16 cells and viable SL2 cells, respectively. Treatment with either reserpine or methysergide resulted in a decreased protection. Delayed-type hypersensitivity (DTH) footpad responses to allogeneic L5178Y (H-2d) tumor cells in C57BL/6 mice showed a biphasic reaction pattern, similar to that found in DTH responses to simple reactive haptens, such as picryl chloride. Moreover, the early swelling responses were also dependent on T cells and on mast cells. BDF1 mice carrying a semisyngeneic L5178Y tumor on the chest showed an early swelling response after footpad challenge but no late response, possibly indicating that selective down regulation of the late component of DTH was associated with progressive tumor growth in these animals. The biphasic patterns of DTH to both tumor cells and picryl chloride and the T cell and mast cell dependence of both antitumor resistance and DTH to tumor cells suggest that T cell-dependent activation of mast cells to allow entry of mononuclear leukocytes into sites of tumor growth is similar to the mechanism that occurs in DTH.
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PMID:A role for mast cells and the vasoactive amine serotonin in T cell-dependent immunity to tumors. 387 Dec 9

R24 is an IgG3 mouse monoclonal antibody that identifies GD3, a prominent ganglioside on the surface of melanoma cells and other cells of neuroectodermal origin. Twelve patients with metastatic melanoma were treated with R24 at three dose levels, 8, 80, or 240 mg/m2, over a period of 2 weeks. Peak antibody levels in the serum were dose related and ranged from less than 0.1 to 62 micrograms/ml. Inflammatory reactions (urticaria, pruritus, erythema, subcutaneous ecchymoses) were observed around tumor sites in patients treated at doses greater than or equal to 80 mg/m2. Tumor biopsies during and after treatment showed lymphocyte and mast cell infiltration, mast cell degranulation, and complement deposition. Side effects were mild and were readily controlled by antihistamines. Major tumor regression has been observed in three patients.
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PMID:Mouse monoclonal IgG3 antibody detecting GD3 ganglioside: a phase I trial in patients with malignant melanoma. 388 55

Fourteen dogs and 11 cats with various malignant tumors were treated daily with benzaldehyde at a dosage rate of 10 mg/kg of body weight, orally, divided into 4 doses. Clinical signs of toxicosis were not observed. A partial response (greater than 50% regression) was observed in animals with an oral squamous cell carcinoma and an oral melanoma. A minimal response (less than 50% regression) was observed in animals with a sweat gland adenocarcinoma and a mast cell sarcoma. One dog with an oral melanoma had stabilization of tumor growth for 8 weeks. Seemingly, benzaldehyde has only minimal anti-tumor activity at the dose studied.
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PMID:Anti-tumor evaluation of benzaldehyde in the dog and cat. 395 33

The relationship of mast cells to tumor growth has been debated but not elucidated. The existence of a mast cell-free animal, the W/Wv mouse, provides a model in which tumor metastasis can be studied with special reference to host tissues and their mast cell content rather than to the adhesiveness of the tumor cell itself. Both hind footpads of 30 W/Wv mice and 30 control mice (+/+) were injected with 2 X 10(5) cells of B16-F10 melanoma cells. The left paw received 1000 rads orthovoltage radiation 12 hr before tumor inoculation. Growth of tumors in both paws was recorded. Ten animals from each group were killed on Day 31 after tumor inoculation, and the remaining animals were kept until they died. Autopsy was performed in all animals, and patterns of metastasis were recorded. Results showed that (1) preinoculation radiation significantly slowed tumor growth in the left paw (P = 0.0009), and (2) lung metastases were present in 4 of 10 W/Wv mice, but in none of 10 +/+ mice killed after 31 days (P = 0.05). Overall, 17 of 25 W/Wv mice and 8 of 26 +/+ mice had lung metastases (P = 0.008).
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PMID:Growth of pulmonary metastases of B16 melanoma in mast cell-free mice. 396 6

The growth rate of Cloudman S91 melanoma cells was compared in groups of normal and immunologically compromised DBA/2 mice that had undergone thymectomy and treatment with antilymphocyte serum. Tumor growth was markedly accelerated in the immunosuppressed animals. Other groups of normal and immunosuppressed animals were treated with daily injections of either histamine, the H-2 antihistamine cimetidine, the H-1 antihistamine pyrilamine; or the mast cell stabilizer proxicromil. Histamine treatment accelerated tumor growth, but only in normal animals and had little effect on tumor growth in immunocompromised hosts. Cimetidine treatment tended to increase tumor growth in normal hosts but this was statistically significant in only 1 of 3 experiments. In contrast, treatment with cimetidine, pyrilamine, or proxicromil always resulted in significant retardation of tumor growth in immunosuppressed animals. These data are consistent with the notion that thymectomy and treatment with antilymphocyte serum results in enhanced tumor growth that is in part due to activation of histamine-dependent suppressor cells. In this system, histamine activation of suppressor cells may be reversed by treatment with either antihistamines or proxicromil, a drug that prevents mast cell release of histamine. However, since the effects of these drugs seem to depend on the immune status of the host, thorough evaluation of immunoregulatory function and careful testing to determine whether histamine blockers reduce or promote tumor growth would seem indicated when immunomodulatory treatment with these drugs is contemplated.
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PMID:The effect of histamine, antihistamines, and a mast cell stabilizer on the growth of cloudman melanoma cells in DBA/2 mice. 686 77

Imexon is an aziridine compound originally studied for immune-enhancing effects on lymphocytes. The drug was well-tolerated in humans and was shown to be active in a variety of animal tumor models. Recently, imexon has demonstrated antitumor activity in human multiple myeloma cell lines in vitro. The pharmacokinetics of the compound using normal phase HPLC assay were studied in normal mice and in dogs with mast cell tumors. Doses of 100 mg/kg given intraperitoneally produced peak plasma levels over 100 micrograms/ml in mice and the drug was rapidly eliminated with half lives of 8 minutes (alpha phase) and 29 minutes (beta phase). Only 20% of an oral imexon dose was absorbed in the mouse. In dogs, the alpha and beta phase half lives ranged from 18-26 minutes and 91-110 minutes, respectively. Peak levels over 100 micrograms/ml were obtained following intravenous doses of 12.5 mg/kg and 25 mg/kg. Imexon was active in mice bearing either P-388 or L-1210 leukemia, but not in mice with B-16 melanoma. These results suggest that cytotoxic drug concentrations can be obtained in vivo and that imexon is active in lymphoproliferative tumors.
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PMID:Preclinical pharmacokinetics and antitumor activity of imexon. 861 72


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