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)

Exposure to tumour cells has previously been shown to induce mast cells to degranulate and release heparin. Isolated mast-cell granules were found to be mitogenic for endothelial cells in vitro. This effect was a property of mast-cell heparin, whose potency as a mitogen exceeded that of commercial heparins. The basis of this difference lay in the proteoglycan structure of the molecule. The release of heparin in mast-cell-tumour co-cultures was examined by both endothelial cell proliferation and isotopic techniques. The kinetics and mode of release are described. The results are discussed in relation to the role of the mast cell in angiogenesis assays and tumour neovascularization.
Int J Cancer 1985 Dec 15
PMID:Mast cells and tumour angiogenesis: the tumor-mediated release of an endothelial growth factor from mast cells. 241 72

The activity of polyethylene glycol 400, a widely used drug solvent, was tested on the release of histamine induced by adriamycin in vitro on peritoneal rat mast cells and in vivo in a mouse model. Preincubation of mast cells with high (10 and 5%) concentrations of polyethylene glycol 400 significantly inhibited the important histamine release induced by 100 micrograms/ml of adriamycin; furthermore, polyethylene glycol 400 (3.45 g/kg; 0.345 g/ml) pretreatment almost completely abolished the peritoneal and pericardial mast cell degranulation and the cardiac toxicity caused by an intraperitoneal injection of 15 mg/kg of adriamycin. This effect of polyethylene glycol 400 on adriamycin-induced histamine release could explain the protective action exhibited in vivo on adriamycin treated animals, therefore confirming that adriamycin cardiotoxicity could be related to the release of histamine and other vasoactive substances.
Eur J Cancer Clin Oncol 1986 Jul
PMID:Effect of polyethylene glycol 400 on adriamycin induced histamine release. 242 41

Immunotoxins--toxins covalently conjugated to specific antibodies--have been studied as possible agents in the treatment of cancer. The avid binding of IgE antibodies to FcR on mast cells and basophils suggested the possible use of an IgE-immunotoxin in the treatment of malignant mastocytosis or as a method to generate mast cell-depleted animals for study. To this end, the effect of a covalent conjugate of rat myeloma IgE and ricin A chain on rat cutaneous mast cells was examined in vivo. IgE-ricin A chain was capable of binding to and sensitizing cutaneous mast cells in vivo as indicated by a bluing response to intracutaneous anti-ricin A chain. IgE-ricin A chain, given either as a single dose or, even more effectively, as two split doses, significantly reduced cutaneous histamine content for 6 to 8 days. Neither a mixture of IgE and ricin A chain that were not conjugated nor the induction of cutaneous mast cell degranulation with anti-IgE affected cutaneous histamine levels. Therefore, IgE-ricin A chain produces a prolonged depletion of cutaneous histamine levels.
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PMID:IgE immunotoxins. Effect of an IgE-ricin A chain conjugate on rat skin histamine content. 244 77

An extremely rare solitary mast cell tumor of the lung was studied histologically, immunohistochemically, and ultrastructurally. The histologic features of the tumor included nodular growth of well-differentiated mast cells and clear cells with no granules. The current case is the third case of a solitary mast cell tumor (granuloma) of the lung in the literature. Clinicopathologic features of this tumor are compared with the other two cases reported previously in the international literature, and the nature of the clear cells is discussed.
Cancer 1988 May 15
PMID:Solitary mast cell tumor of the lung. 245 7

Epirubicin induces an important noncytotoxic release of histamine from rat peritoneal cells in vitro. This exocytotic response is inhibited by sodium cromoglycate, similarly to that elicited by the classic mast cell secretagogue, compound 48/80. Mast cells obtained from the peritoneal cavities of rats treated with epirubicin in vivo were extensively degranulated; in contrast, samples obtained from rats pretreated with sodium cromoglycate showed normal appearing mast cells. When injected i.p., immediately before the antineoplastic agent, cromolyn significantly improved the survival time and the microscopic appearance of myocardial tissues of epirubicin-treated mice. The results indicate that histamine release could play an important role in the pathogenesis of anthracycline-induced cardiotoxicity.
Eur J Cancer Clin Oncol 1989 Feb
PMID:Amelioration of 4'-epidoxorubicin-induced cardiotoxicity by sodium cromoglycate. 246 9

The average number of nucleolar organiser regions per cell has previously been shown to correlate well with histological grading techniques for a variety of neoplasms in man, and may thus be of value as an aid to post-surgical prognosis. In this study 50 spontaneously arising, subcutaneous canine mast cell tumours were graded and the histological grade compared with the mean AgNOR count. For well differentiated neoplasms the mean count was 1.4 per cell compared with 6.3 for poorly differentiated neoplasms, while tumours of intermediate differentiation had a mean count of 3.2 per cell. Subsequent follow up studies revealed that the AgNOR count was an accurate prognostic indicator, 73% of dogs with a high mean count (greater than 4.9) being destroyed from tumour related disease compared with 33% with an intermediate count (1.7-4.8). No dog with a count of less than 1.7 has been destroyed because of tumour recurrence to date and the AgNOR count has proved to be a better and more objective prognostic indicator than either histological tumour grade or mitotic index. Since most dogs which develop recurrent mast cell tumours do so within 6 months of initial surgery, an assessment of the predictive value of AgNORs can be obtained more quickly in canine tumours than for comparable human neoplasms.
Br J Cancer 1989 Jun
PMID:Nucleolar organiser regions as indicators of post-surgical prognosis in canine spontaneous mast cell tumours. 250 Jan 45

Although the association of malignancies and systemic mast cell disease (SMCD) is well established, the nature of this relationship is poorly understood. The observation of 19 malignancies in 17 of 60 patients with SMCD raised several questions regarding the chronological relationship of onset of SMCD and the malignancies, whether these patients are at increased risk for developing malignancy, and whether the distribution of solid vs hematologic malignancies indicates a relationship between SMCD and a particular tumor. The following malignancies were observed: eight solid tumors, seven acute nonlymphocytic leukemias, three malignant lymphomas, and one refractory anemia with excess blasts in transformation. The majority (13/17) of patients were found to have malignancies before, or within 12 months of, SMCD diagnosis. Statistical analysis suggested that patients with SMCD are not at increased risk for malignancies subsequent to the diagnosis of SMCD. The varied types of solid malignancies observed indicated a random distribution, in contrast to the hematologic malignancies that appeared to primarily affect the myeloid cells.
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PMID:Solid and hematologic malignancies in 60 patients with systemic mast cell disease. 265 Jun 53

Splenomegaly confirmed by surgery or necropsy in 100 dogs was diagnosed histologically as benign neoplasia (n = 1), primary splenic malignancy (n = 59), neoplastic metastases (n = 6), and nonneoplastic disease (n = 34). Dogs with known systemic disease, such as lymphoma and mast cell tumor, that caused splenomegaly were not included in the study. Hemangiosarcoma was the most common splenic disease (43 cases). Overall mean age of the dogs was 10.7 years, the most common breed was German Shepherd dog, and 72 of the dogs weighed more than 21 kg. Dogs with anemia, nucleated red blood cells, abnormal red blood cell morphology, or splenic rupture had a significantly greater chance of having splenic neoplasia (P less than 0.002). A multivariable logistic regression analysis found that the presence of anemia and splenic rupture in dogs with splenomegaly was up to 69% accurate in predicting presence of splenic neoplasia. After splenectomy, the median survival time of dogs with splenic neoplasia was 13 weeks. For dogs with nonneoplastic splenomegaly it was at least 36 weeks.
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PMID:Splenomegaly in dogs. Predictors of neoplasia and survival after splenectomy. 277 49

We have constructed a transgenic mouse strain in which a mammary tumor virus LTR/c-myc fusion gene is anomalously expressed in a wide variety of tissues. The deregulated c-myc transgene, now glucocorticoid inducible, contributes to an increased incidence of a variety of tumors, including those of testicular, breast, lymphocytic (B cell and T cell), and mast cell origin. The deregulated gene does not, however, otherwise disturb cell proliferation, nor does it interfere with normal development in these animals. Moreover, since not all tissues that express the transgene develop neoplasms, these results begin to define the transforming spectrum of the c-myc oncogene. They also extend to several organ systems the notion that elements in addition to an activated c-myc gene are required to induce malignancy in the living organism.
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PMID:Consequences of widespread deregulation of the c-myc gene in transgenic mice: multiple neoplasms and normal development. 301 Dec 71

Significant numbers of mast cells have been demonstrated histologically around the periphery of the invasive rat mammary adenocarcinoma 13672NF. The number of mast cells at microfoci along the tumour:host tissue junction was significantly greater than that found in normal mammary tissues, and few mast cells were detected within the tumour itself. Mast cell degranulation, often associated with disruption and lysis of the connective tissue matrix, was a common feature in later stages of tumour proliferation. When soluble products derived from purified rat peritoneal mast cells were added to monolayer cultures of rat stromal fibroblasts or tumour cells they stimulated a significant increase in total collagenase production, and the mast cell products were also capable of activating the latent collagenases thus produced. Histological examination indicated that degradation of local collagenous matrix was a common feature of mast cell degranulation, an observation possibly explained by the release of mast cell enzymes and/or the potential of this cell to modulate the expression of collagenolytic activity by surrounding cells. These observations suggest that, at least in some tumours, mast cells contribute to the connective tissue breakdown commonly associated with tumour invasiveness and metastatic spread.
Br J Cancer 1986 Sep
PMID:Mast cells and matrix degradation at sites of tumour invasion in rat mammary adenocarcinoma. 301 77


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