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)

Three hundred and two carcinomas of the female breast were studied histologically with special reference to the morphologic aspects of the tumor, its surrounding host tissue and the regional lymph nodes. The nuclear grade of the tumor was positively correlated with the five year survival rate of the patient. Tumor metastases in the regional lymph nodes were observed to be a sign of a poor prognosis. The stromal lymphocyte and mast cell reactions did not correlate with the frequency of nodal metastases or the five year survival rate. Sinus histiocytosis in the lymph nodes was a sign of favorable five year survival because of its presence in cancer-free nodes only. The paracortical activity of the lymph nodes was an important determinant of whether or not tumor metastases appear in the node.
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PMID:Tumor-host interrelationships in carcinoma of the female breast. 66 8

One hundred and thirty eight gastric carcinomas were studied histologically with special reference to the morphology of the tumor, its surrounding tissues and the regional lymph nodes. A special search was focused on the morphologic manifestations of possible host factors in association with gastric carcinoma. The most prominent findings were as follows: 1. The nuclear grade of the tumor was positively correlated with the 5-year survival rate of the patients. 2. The content of tumor-derived mucus was not a prognostic determinant. 3. The intensity of the stromal lymphocyte and plasma cell reactions did not affect the prognosis but was inversely related to the frequency of nodal metastases. 4. Sinus histiocytosis and nodal mast cell reactions were an important determinant of whether nodal metastases appear or not. 5. An active paracortical area of the lymph node was almost incompatible with the appearance of nodal metastases.
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PMID:Prognostic factors in gastric carcinoma. 68 79

Aldose reductase was visualized by light and electron microscopy using a goat anti-rat antibody with immunoperoxidase and immunogold, respectively. Ouabain-sensitive, K(+)-dependent, p-nitro-phenylphosphatase, a component of (Na+, K+)-ATPase, was localized at the electron microscopic level by enzyme histochemistry using p-nitro-phenylphosphate as substrate. In peripheral nerve, spinal ganglia and roots, the Schwann cell of myelinated fibers was the principal site of aldose reductase localization. Immunostaining was intense in the paranodal region and the Schmidt-Lanterman clefts as well as in cytoplasm of the terminal expansions of paranodal myelin lamellae and the nodal microvilli. Schwann cell cytoplasm of unmyelinated fibers were faintly labelled. Endoneurial vessel endothelia, pericytes and perineurium failed to bind appreciable amounts of aldose reductase antibody. However, mast cell granules bound antibody strongly. In contrast, p-nitro-phenylphosphatase reaction product was detected in the nodal axolemma, terminal loops of Schwann cell cytoplasm and the innermost layer of perineurial cells. In endothelial cells, reaction product was localized on either the luminal or abluminal, or on both luminal and abluminal plasmalemma. Endothelial vesicular profiles were often loaded with reaction product. Occasional staining of myelin and axonal organelles was noted. Mast cells lacked reaction product.
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PMID:Fine-structural localization of aldose reductase and ouabain-sensitive, K(+)-dependent p-nitro-phenylphosphatase in rat peripheral nerve. 165 Jan 13

1. The effects of mast cell degranulating peptide (MCDP), a toxin from the honey bee, and of dendrotoxin (DTX), a toxin from the green mamba snake, were studied in voltage-clamp experiments with myelinated nerve fibres of Xenopus. 2. MCDP and DTX blocked part of the K+ current. About 20% of the K+ current, however, was resistant to the toxins even in high concentrations. In Ringer solution half-maximal block was reached with concentrations of 33 nM-MCDP and 11 nM-DTX. In high-K+ solution the potency of both toxins was lower. beta-Bungarotoxin (beta-BuTX), another snake toxin, also blocked part of the K+ current, but was less potent than MCDP and DTX. 3. Tail currents in high-K+ solution were analysed and three K+ current components were separated according to Dubois (1981 b). Both MCDP and DTX selectively blocked a fast deactivating, slowly inactivating K+ current component which steeply activates between E = -60 mV and E = -40 mV (component f1). In concentrations around 100 nM, MCDP and DTX blocked neither the slow K+ current (component s) nor the fast deactivating, rapidly inactivating K+ current which activates between E = -40 mV and E = 20 mV (component f2). Similar results could be derived from K+ outward currents in Ringer solution. In high-K+, IC50 of MCDP for component f1 was 99 nM, whereas it was 7.6 microM for f2. Corresponding values for DTX are 68 nM and 1.8 microM. 4. Binding studies with nerve fibre membranes of Xenopus reveal high-affinity binding sites for 125I-labelled DTX (KD = 22 pM in Ringer solution and 81 pM in high-K+ solution). 125I-labelled DTX can be displaced from its sites completely by unlabelled DTX, toxin I (black mamba toxin), MCDP, and partially by beta-BuTX. 5. Immunocytochemical staining demonstrates that binding sites for DTX are present in nodal and paranodal regions of the axonal membrane. 6. The axonal membrane of motor and sensory nerve fibres is equipped with three types of well-characterized K+ channels and constitutes so far the best preparation to study MCDP- and DTX-sensitive K+ channels with electrophysiological and biochemical methods.
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PMID:A K+ channel in Xenopus nerve fibres selectively blocked by bee and snake toxins: binding and voltage-clamp experiments. 232 90

Reports vary on the amount and distribution of mast cells in lymph nodes. We analysed the mast-cell population in compartments of nodes of diverse sites, from euthymic and athymic animals of various ages. Nodal mast cells were few in young animals, occurring mostly in medullary sinuses. Aging is often accompanied by a moderate increase of nodal mast cells. In compartments of a few nodes of some aged athymic and euthymic animals, the mast cells were greatly increased in the extrafollicular zone overlying medulla directly. In certain cases, this great increase was accompanied by pronounced mast-cell degranulation and by fibrosis in the mast cell-rich extrafollicular zone. It is suggested that the mast cells of medullary sinuses relate to non-immunological events, while those of the lymphoid parenchyma relate to elements that can induce humoral immune responses or are somehow involved in nodal processes of such responses. It is further suggested that an occasional emergence, with aging, of a deficiency of particular humoral immune responses may induce an excessive increase of cortical mast cells, and that activities of the resulting dense mast-cell population contribute to the onset of fibrosis.
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PMID:Mast cells and fibrosis in compartments of lymph nodes of normal, gnotobiotic, and athymic rats. 238 81

The frequency distribution of tissue mast cells and eosinophilic granulocytes in tumor-draining lymph nodes was evaluated. In total 483 axillary lymph nodes draining invasive ductal breast cancer and 162 paracolic lymph nodes draining infiltrating adenocarcinoma of the large bowel were analyzed. Significantly higher number of sinus mast cells were found in axillary lymph nodes as compared with the paracolic ones whereas eosinophilic granulocytes were more frequent in paracolic than in axillary lymph nodes. Concerning both cell systems no significant differences could be demonstrated when all lymph nodes from nodal-negative cases were compared with the lymph nodes from cases with regional lymph node metastases. Tumor-free axillary lymph nodes, however, showed a significantly higher mast cell content in the sinus and medulla than did lymph nodes bearing metastases. The number of eosinophilic granulocytes did not differ in either lymph node group.
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PMID:Frequency distribution of tissue mast cells and eosinophilic granulocytes in tumor-draining axillary and paracolic lymph nodes. 377 24

In breast carcinoma metachromasia on staining the primary tumour with toluidine blue is related to mast cell changes and an infiltrative as opposed to an expansive growth form. In 73 patients the presence of metachromasia in the zone of host-tumour interaction, just beyond the edge of the tumour cells, was associated with poor short-term survival, giving greater discrimination than, for example, axillary nodal status or histological grade. 12 of 19 patients with metachromasia in this zone died within 5 years of operation. This indicates that the reaction is not only related to local infiltrative growth, but may also reflect the tumour potential for metastatic spread. In the absence of metachromasia in this zone death occurred mainly in patients with poorly differentiated tumours. The possible mechanisms involved are discussed. It is stressed that stromal metachromasia is not tumour specific, but that in certain areas, under defined circumstances, it may give information of both prognostic and biological interest.
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PMID:Mast cell changes and tumour dissemination in human breast carcinoma. 620 34

BACKGROUND: Increased numbers of mast cells are found in various solid tumors. To investigate the role of mast cells in the vicinity of gastric cancer cells, we used special staining and an immunohistochemical technique.METHODS: Specimens were surgically obtained from 102 patients with gastric cancer. Mast cells around the tumor edge of gastric cancer nests were counted by staining with 0.05% toluidine blue solution. Blood vessels in these areas were also counted, by immunohistochemical staining of endothelial cells for factor VIII.RESULTS: The average number of mast cells and blood vessels in gastric cancer specimens was significantly higher than that in normal gastric tissue. Specimens from patients with advanced disease with metastases to lymph nodes had more mast cells than specimens from patients with early-stage disease. Mast cells in specimens from patients with metastatic lymph nodes were significantly increased in comparison with numbers in specimens from those without nodal metastases. Mast cell numbers in the specimens of patients with lymphatic or blood vessel invasion were significantly higher than numbers in specimens from patients without such invasion. Mast cells were localized near the new vessels around gastric cancer cells. Mast cell numbers increased as the number of blood vessels increased (correlation coefficient, 0.783). Postoperative survival curves revealed that patients with increased numbers of mast cells had a poor prognosis.CONCLUSIONS: All these results suggest that mast cell accumulation at the tumor site may lead to increased rates of tumor vascularization and, consequently, increased rates of tumor growth and metastasis.
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PMID:Mast cell infiltration around gastric cancer cells correlates with tumor angiogenesis and metastasis. 1195 67

The principles of the new WHO classification of haematopoietic and lymphoid tumours are based on those defined in the Revised European American classification of Lymphoid neoplasms (REAL), published by the International Lymphoma Study Group (ILSG) in 1994. Thus, the new WHO classification may be considered an updated version of the REAL classification rather than of the old WHO classification published in 1976. Disease entities are defined on the basis of morphological, phenotypic, genotypic, and clinical data. The relative impact of these characteristics varies among different diseases and there is "no gold standard". Thus, the strict hierarchy among diagnostic criteria, headed by morphology and followed by immunohistochemistry and genetics, has been discontinued. The WHO classification not only encompasses lymphoid tumours but extends to myeloid, mast cell and histiocytic/dendritic cell malignancies. Neoplasms are primarily stratified according to their tumour cell lineage. For each neoplasm a cell of origin is postulated. The classification of lymphoid malignancies recognises three major categories, B-cell neoplasms, T-/NK-cell neoplasms, and Hodgkin lymphomas. B-cell and T-cell lymphomas are further divided into precursor neoplasms and mature neoplasms, the latter being subdivided according to their clinical manifestation into disseminated/leukaemic, extranodal and nodal malignancies. In contrast to previous classifications, the neoplasms are grouped neither according to their histological grade (Kiel classification) nor according to their clinical aggressiveness (International Working Formulation). However, the histological grade is considered a prognostic factor which enters into the description of each disease entity. Hodgkin's disease, now more appropriately termed Hodgkin lymphoma, comprises nodular lymphocyte-predominant Hodgkin lymphoma and classical Hodgkin lymphomas of nodular sclerosis, mixed cellularity, lymphocyte-depleted and lymphocyte-rich subtype. For practical purposes this minireview disregards the description of myeloid, macrophage/histiocytic, dendritic cell and mast cell disorders. Furthermore, the present paper is restricted to those lymphoid tumours that are not already identically described in the REAL classification, in order to focus on what is really new in the WHO classification.
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PMID:Who is WHO and what was REAL? 1258 44

Palpable swelling of regional lymph nodes is a common sequela of microbial infections but the mechanism responsible for the sequestration and subsequent coordination of lymphocyte responses within these dynamic structures remains poorly understood. Here we show that draining lymph nodes of mast cell-deficient mice did not demonstrate swelling after intradermal bacterial challenge. Testing of individual mast cell-derived products in this model indicated that tumor necrosis factor was the main mediator of nodal hypertrophy, whereas tryptase and histamine had no effect. After peripheral mast cell activation, both tumor necrosis factor concentrations and the recruitment of circulating T cells were increased within draining nodes. These results show a critical function for peripheral mast cell-derived tumor necrosis factor in regulating the hypertrophy of draining lymph nodes during infection.
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PMID:Mast cell-derived tumor necrosis factor induces hypertrophy of draining lymph nodes during infection. 1463 63


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