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)

A 57-year-old female patient, admitted for an acute abdominal syndrome, was found to have an extensive proliferation of mast cells both in the peripheral blood and the bone marrow. Cytochemical studies confirmed the mast cell characteristics of the pathological cell population, while the immunophenotype strongly suggested a bone marrow origin of this malignancy. The course of the disease was not affected by antiproliferative treatment and the patient, after progressive general deterioration, died of intractable haemorrhage. On both clinical and haematological criteria it seems possible to distinguish this rare case of primary mast leukaemia from the more common form of tissue mastocytosis with secondary leukaemia.
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PMID:Mast cell leukaemia: evidence for bone marrow origin of the pathological clone. 309 68

We counted the number of toluidine blue positive mast cells within and around the tumor in 44 patients with soft tissue sarcomas (STS). Irrespective of their histologic types, these cases were broadly divided into the following two groups: (1) low count (less than 20 mast cells/10 high-power fields [HPF]) and (2) high count (greater than or equal to 20 mast cells/10 HPF). The patients with a high mast cell count showed a significantly better 5-year survival rate than those with a low count (85.9% versus 30.5%; P less than 0.01). Five patients with distant metastases at first admission all belonged to the low count group. These results suggest that the number of mast cells within and around the tumor is a useful prognostic factor for STS.
Cancer 1988 Dec 01
PMID:Prognostic significance of mast cells in soft tissue sarcoma. 317 60

The accumulation of malignant ascites is a significant cause of morbidity and mortality in patients with intraabdominal malignancies. However, the cause of malignant ascites is unknown. In this study, we used the rat cremaster muscle preparation to determine if and how malignant ascites could produce protein leakage from normal blood vessels which would lead to fluid accumulation in the peritoneal cavity. The rat cremaster muscle, with nerves and blood vessels to the animal intact, was prepared for microscopic observations of the microcirculation. Serum albumin was tagged to fluorescein isothiocyanate and injected into the rat. Fluorescent microscopy was used to quantitate leakage of the tagged albumin into the interstitial tissue. Malignant ascites was collected from a patient with metastatic breast cancer. The ascites fluid was placed on the cremaster muscle and it induced protein leakage from the normal blood vessels of this tissue. Protein leakage was partially blocked by diphenhydramine (10(-4) M) and by mast cell depletion with compound 48/80. There was a high level of C3a in the malignant ascites solution but C3a did not increase during the exposure period. These data suggest that activated complement in malignant ascites may release histamine from mast cells to cause protein leakage of the normal vasculature. The movement of protein into the peritoneal cavity would be followed by water, thus increasing the volume of the ascites and exacerbating the clinical condition.
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PMID:Human malignant ascites and histamine-induced protein leakage from the normal microcirculation. 325 8

We found that prolactin is taken up by mast cells residing in prolactin-dependent, 7,12-dimethylbenzanthracene-induced rat mammary tumors. Light and electron microscopic immunocytochemistry showed that mast cells concentrate prolactin in their cytoplasmic granules. No prolactin was found on mast cell surface membranes or in their nuclei. In primary cultures of tumor cells, mast cells were found mainly in the periphery of dome structures and these cells concentrated prolactin. When purified rat peritoneal mast cells were incubated with 125I-labeled prolactin, uptake was time, energy, and temperature dependent. Seventy % of accumulated prolactin was released intact from cytoplasmic granules by C48/80-induced degranulation. A mouse mastocytoma cell line also took up and released prolactin. These cells contained prolactin receptors (Kd = 4.5 nM) as determined in whole cells (approximately 3150 sites/cell) and in crude membranes (approximately 180 fmol/mg protein). We conclude that mast cells might significantly influence mammary tumor growth by accumulating and releasing prolactin within tumor tissue.
Cancer Res 1988 Jul 01
PMID:Prolactin binding and localization in rat mammary tumor mast cells. 328 35

A clinical and hematopathologic review of 66 patients with systemic mast cell disease (SMCD) was undertaken to investigate the frequency and the clinical significance of associated hematologic disorders. Twenty-two patients were found to have a second hematologic disorder, 19 of which involved the myeloid cells (ten dysmyelopoietic syndromes, five myeloproliferative disorders, three acute nonlymphocytic leukemias, and one chronic neutropenia), and three of which involved the lymphoid cells (three malignant lymphomas). A chromosome analysis of the bone marrow revealed abnormalities characteristic of neoplastic myeloid disorders in four patients. Five-year survival for patients with hematologic disorders was 28% compared with 61% for other SMCD patients (P = 0.004). Patients with hematologic disorders differed significantly from other SMCD patients in that they were about 7 years older (P = 0.039), and they presented more commonly with anemia (P less than 0.001) and constitutional symptoms (P = 0.007). These patients also had less frequent skin symptoms (P = 0.003) and urticaria pigmentosa (P = 0.018). By definition, patients with hematologic disorders had a greater percent of hematopoiesis (P less than 0.001) and decreased fat cells (P = 0.011) on bone marrow biopsies. A multivariate model demonstrated that the following independent variables were associated with the presence of hematologic disorders: low hemoglobin (P = 0.001), the absence of hepatomegaly (P = 0.016), high leukocyte count (P = 0.021), and the presence of pathologic fractures (P = 0.051). The frequent coexistence of SMCD with dysplastic and neoplastic disorders of myeloid cells is consistent with the concept that SMCD itself is a disorder of myeloid cells and that the mast cell may be myeloid in origin.
Cancer 1988 Sep 01
PMID:Significance of systemic mast cell disease with associated hematologic disorders. 340 77

Morphologic, histochemical, biochemical and morphometric procedures were employed for examination of resected regional lymph nodes obtained from 70 patients suffering various malignancies. The important role of blood microcirculation bed alterations in cancer dissemination was established, the said disorders being as follows: decreased functional activity of the vascular wall and its increased permeability matched by intravascular blood coagulation and extravascular deposition of large amounts of fibrin in the lymph node tissue. Those changes were largely determined by lymph node mast cell reaction and levels of histamine and serotonin in the lymph node tissue. They preceded lymph node involvement.
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PMID:[The role of microcirculatory factors in cancer metastasis]. 342 Aug 36

Interleukin 4 (IL-4) expresses multiple biologic activities, including B cell, mast cell, and T cell stimulation. We showed that the incubation of resting splenocytes from C57BL/6 mice solely in purified native or recombinant mouse IL-4 results in the generation of lymphokine-activated killer (LAK) activity directed against fresh, syngeneic sarcoma cells. The precursor activated by IL-4 expresses surface asialo-GM1. In addition, IL-4 is capable of amplifying the splenic LAK activity induced by recombinant IL-2. The generation, by IL-4, of killer cells with broad antitumor reactivity raises the possibility of using IL-4 alone or in combination with IL-2 in the immunotherapy of cancer in animal models.
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PMID:Interleukin 4 (B cell stimulatory factor 1) can mediate the induction of lymphokine-activated killer cell activity directed against fresh tumor cells. 349 2

A series of 70 patients with the squamous cell carcinoma of the lip and followed-up for at least 5 years, was assessed on light microscopy and using histochemical staining for ANAE (acid-naphthyl acetate esterase) to demonstrate the morphological manifestations of tumor-host reactivity. The factors analysed include cancer differentiation (intrinsic malignancy) and stromal reactions (intensity of the immunocompetent cell infiltrate including the mast cells and the subpopulations, i.e. B- or T lymphocytes or mononuclear phagocytes). Differentiation of the lip cancer was shown to be directly (although not statistically significantly) related to the 5-year survival, as was also the intensity of the stromal immunocompetent cell infiltration. Cancer metastases were evidently the most powerful prognostic determinants, their development being influenced both by the intensity of the stromal immunocompetent cell infiltrate and cancer differentiation. B lymphocytes far outnumbered the T and MPS cells in all the infiltrates studied, the percentages of the latter two cell types, however, being inversely related to the intensity of the infiltrate. The cell composition in the infiltrates was seemingly without effect on the frequency of metastases and the 5-year survival, as was the stromal mast cell reaction, too. It was concluded that analysis of tumor-host relationships using a variety of morphological and immunohistochemical techniques may be of benefit in predicting the clinical course of lip cancer.
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PMID:Tumor differentiation and tumor-host interactions as prognostic determinants in squamous cell carcinoma of the lip. 351 41

An intimate interplay between the host factors and the tumour seems to be operative in lip cancer, and is undoubtedly capable of modifying the clinical course of the disease. A series of 70 patients with squamous cell carcinoma of the lip was assessed by light microscopy and using histochemical staining for acid alpha-naphthyl acetate esterase to demonstrate the morphological manifestations of tumour-host reactivity. The factors analysed include stromal reactions; intensity of the immunocompetent cell infiltrate including mast cells, and the subpopulations, i.e. B or T lymphocytes and mononuclear phagocytes (MPS cells). B lymphocytes far outnumbered the T and MPS cells in all the infiltrates studied, the percentages of the latter two cell types being inversely related to the intensity of the infiltrate, however. The cell composition in the infiltrates lacked statistically demonstrable effect on the frequency of metastases and the 5-year survival, as did the stromal mast cell reaction, too.
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PMID:Immunocompetent cell reaction in prognostic evaluation of squamous cell carcinoma of the lip. 361 94

We have previously reported that rodent tumor cell lines secrete a potent vascular permeability factor with a molecular weight of 34,000-42,000 (Senger et al. Tumor cells secrete a vascular permeability factor that promotes accumulation of ascites fluid. Science (Wash. DC), 219: 983-985, 1983). This tumor-secreted vascular permeability factor (VPF) causes a rapid and completely reversible increase in microvascular permeability in the species (guinea pig or rat) from which the tumors were derived without causing mast cell degranulation or endothelial cell damage or exciting an inflammatory cell infiltrate. This VPF may be responsible, at least in part, for the increased permeability which is commonly displayed by solid and ascites tumor vessels. We have now examined 7 human tumor cell lines and have determined that 5 of them also secrete this same VPF. Antibody raised to guinea pig line 10 VPF neutralized more than 90% of the vascular permeability-increasing activity secreted by these 5 human tumor lines. Furthermore, VPFs from both guinea pig and human tumor sources bound to and were eluted similarly from immobilized heparin and comigrated identically on sodium dodecyl sulfate-polyacrylamide gels. Finally, 2 tumorigenic (in nude mice) human cell lines were found to secrete at least 14-fold more VPF than their directly matched, nontumorigenic counterparts, suggesting that elevated expression of this permeability factor may correlate with neoplastic transformation. These data suggest that a broad spectrum of tumor cells from several species, including humans, secretes a highly conserved molecule that enhances local vascular permeability and that this function may be important for tumor growth.
Cancer Res 1986 Nov
PMID:A highly conserved vascular permeability factor secreted by a variety of human and rodent tumor cell lines. 375 10


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