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

A West Indian man who was infected with Strongyloides stercoralis developed small intestinal obstruction. Treatment with thiabendazole did not relieve the obstruction which was found at laparotomy to be due to a poorly differentiated small intestinal lymphoma. There was no blood eosinophilia or accumulation of eosinopohils in the sites of infection. There was no reaction in the skin to delayed hypersensitivity antigens and the blood T lymphocyte count and serum C3 levels were low. From these findings and a review of the literature it was concluded that the immune response in man to Strongyloides stercoralis may depend on T lymphocyte mediated reactions including granuloma formation, and mast cell and eosinophil responses in tissues. We suggest that the association of strongyloides hyperinfection and small bowel lymphoma in this patient may not have been fortuitous. The lymphoma may have led to a reduction in cellular immunity, with the subsequent development of strongyloides hyperinfection.
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PMID:Strongyloides stercoralis infection and small intestinal lymphoma. 31 39

The de novo megakaryocytic leukemia fulfilling the FAB criteria is still an uncommonly recognized variant of acute leukemia. Many studies have shown that the megakaryocytic leukemic events may occur at a pluripotent stem cell level and clinical observations reveal that the megakaryocytic leukemias are diverse entities. The immunophenotyping using monoclonal antibodies against platelet specific surface antigens and the ultrastructural detection of platelet peroxidase reaction do not provide sufficiently useful information to determine whether a megakaryocytic leukemia is chronic, acute, therapy-responsive or therapy-unresponsive. More sophisticated techniques are required to further characterize megakaryocytic leukemic cells. In this review, we emphasize that megakaryocytic leukemic cells can be categorized into two groups; one with the PF4 mRNA, and the other without it, and that the expression of PF4 mRNA in the blasts could be a useful marker for the identification of mature megakaryoblasts. It seems that the patients with blasts expressing PF4 mRNA will have a longer survival and a better response to chemotherapy than those without PF4. We further discuss the fact that the detection of mRNAs of the IL-6 receptor, PDGF A- and B-chains, and TGF beta 1 in megakaryocytic leukemic cells will be useful to clarify the mechanisms involved in the proliferation of megakaryocytic leukemic cells and fibroblasts in the bone marrow. Furthermore, we reviewed data showing that megakaryocytic erythroid, and mast cell lineages share the nuclear transcription factor known as GF-1 (NF-E1 or Erf-1). We suggest that characterization of megakaryocytic leukemia should be performed using monoclonal antibodies against erythroid, megakaryocytic and mast cell lineages.
Leuk Lymphoma 1992 Nov
PMID:Megakaryocytic leukemia and platelet factor 4. 133 50

The noncytotoxic rat mast cell tumor line RBL was transfected with genes for the cytotoxic lymphocyte granule proteins cytolysin (perforin) and granzyme A, giving transfectants with mRNA and protein expression levels comparable with cloned cytotoxic T lymphocytes. Both RBL-cytolysin and RBL-cytolysin-granzyme A transfectants showed extremely potent killing of red cell targets and lysed 20%-60% of EL4 lymphoma targets at an effector-to-target ratio of 30. RBL transfectants expressing only granzyme A were not cytotoxic. Significant EL4 DNA breakdown accompanying lysis was observed only with RBL that was transfected with both cytolysin and granzyme A. These results support the granule-exocytosis model for lymphocyte cytotoxicity and show that effector granzyme A plays a role in target cell DNA breakdown.
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PMID:Cytotoxicity with target DNA breakdown by rat basophilic leukemia cells expressing both cytolysin and granzyme A. 142 96

Generalised mastocytosis is a rare condition characterised by the clinical features of the release of vasoactive peptides from tissue mast cells infiltrating in the reticuloendothelial tissues. The mast cell however appears to have its origin in the pluripotential bone marrow stem cell committed to a basophil and it is therefore not surprising that myeloproliferative and myelodysplastic disorders commonly co-exist or terminate the clinical phase of mastocytosis. Both abnormal proliferation and maturation of the myeloid committed cells are found. Non-Hodgkin's lymphoma can occur before and after mastocytosis becomes manifest. While this is statistically a random event the relationship between lymphokines and mast cell differentiation and proliferation raises the possibility of a benign reactive lymphoid event eventually becoming malignant.
Leuk Lymphoma 1992 May
PMID:Mastocytosis and co-existent non-Hodgkin's lymphoma and myeloproliferative disorders. 147 31

The mast cell, equipped with enzymes, chemotactic factors, a vasoactive amine, an anticoagulant, and lipid-derived proinflammatory products, may be essential in tissue modeling as well as in defense. Its primarily perivascular location in skin and the mucosa of the respiratory tract and the gut assures its availability to counter parasites. By the same token, the mast cell is responsible for interactions with inhaled, ingested, and injected antigens that comprise IgE-mediated allergic reactions. Abnormally high numbers of mast cells in the skin, either localized or generalized, result in urticaria pigmentosa or generalized cutaneous mastocytosis, respectively. Tissue infiltration by excessive mast cells, primarily in gut, bone, liver, and spleen, results in systemic mastocytosis; this may be accompanied by myelodysplasia or lymphoma and may eventuate in mast cell leukemia. Until the etiology of mastocytosis is understood, the treatment is symptomatic: histamine antagonism by H1 +/- H2 blockade for flushing, itching, and gastric distress; cyclooxygenase inhibition to prevent prostaglandin D2 (PGD2)-induced hypotension when indicated; and oral cromolyn to prevent gastrointestinal symptoms and bone pain.
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PMID:Mast cell disease. 149 Jun 22

A survey of the occurrence of mast cell tumours in CD-1 mice (Caesarian derived) recorded nine tumours in 24352 mice used for carcinogenicity studies over a period of six years (1984-1989). All except one appeared as multi centric tumours. Three of the mice had deposits only in the bone marrow, one of those cases was associated with intestinal adenocarcinoma and harderian gland adenoma. Case four had deposits in lung, thymus, lymph nodes, liver, spleen and kidney and occurred in association with pulmonary adenocarcinoma and pleomorphic lymphoma. Case five showed the tumour deposits in mesenteric lymph nodes and liver. Case six showed deposits of the tumour in lung, liver, kidney and bone marrow and in this case there was also a cutaneous fibrosarcoma. Case seven was diagnosed as mast cell leukaemia. Case eight was a subcutaneous tumour, case nine showed subcutaneous deposits and deposits in lungs, lymph nodes, liver, spleen and bone marrow.
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PMID:Mast cell tumours in CD-1 mice. 190 30

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

Blood findings in 61 cases of generalized mastocytosis (GM) were evaluated. The cases were divided into two major variants: Systemic mastocytosis (SM; n = 34) with urticaria pigmentosa-like skin lesions, and malignant mastocytosis (MM; n = 27), without skin involvement. The following results were obtained: (1) Significant differences between MM and SM were found in the main haematological parameters (erythrocyte, platelet and leucocyte counts and haemoglobin level); normal values were found in 16 of the SM cases, but never in MM. (2) The main pathological findings were: in SM, anaemia (9/34) and leucocytosis (5/34); and in MM, leucocytosis (19/27), monocytosis (14/27), eosinophilia (12/27), bicytopenia (12/27, mostly anaemia with thrombocytopenia), basophilia (10/27) and isolated anaemia (7/27). (3) The major finding was a significant difference between MM and SM in the incidence of myeloproliferative disorders (MPD), myelodysplasia and mast cell leukaemia (MCL): these disorders occurred in 23 (92%) MM patients, but only in two (6%) SM patients (P less than 0.001). The four instances of MCL and two of myelodysplasia all occurred with MM. Of the 19 cases of MPD, six (SM, 1; MM, 5) were acute variants (acute myeloid and myelomonocytic leukaemias) and 13 (SM, 1; MM, 12) were chronic variants. No case of malignant lymphoma was noted. (4) The blood picture in 10 of 13 chronic MPD cases represented an atypical chronic myeloid leukaemia for which the preliminary descriptive term 'mastocytosis-associated MPD' is proposed. (5) A survey of 103 published cases (SM, 77; MM, 26) yielded similar findings, including a high incidence of MPD and MCL in MM. These findings add further weight to the argument for recognizing SM and MM as two separate entities.
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PMID:Blood findings in generalized mastocytosis: evidence of frequent simultaneous occurrence of myeloproliferative disorders. 201 71

The records of 26 patients with systemic mast cell disease (SMCD) treated during the past decade at the National Institutes of Health were reviewed to determine the role of splenectomy in the management of SMCD. Seventeen (65%) patients had indolent SMCD, manifested primarily by urticaria pigmentosa and mast cell infiltration of the skin, bone marrow, or gastrointestinal tract. None of these patients underwent splenectomy. These patients required only symptomatic therapy. Nine (35%) patients, including those with associated hematologic disorders and those with a lymphoma-like illness termed lymphadenopathic mastocytosis with eosinophilia, had aggressive SMCD. Five of nine patients with aggressive SMCD underwent splenectomy. Of the five patients with splenectomy, three were alive at the time of this report, whereas none of the four who did not have a splenectomy was still alive. Length of survival without splenectomy was 26 months. With splenectomy, length of survival at the time of this report was 34 months. Patients without splenectomy died of bleeding caused by severe thrombocytopenia. Patients with splenectomy appeared better able to tolerate chemotherapy. We thus conclude that while splenectomy is of no value in the management of indolent mastocytosis, it should be considered in patients with aggressive SMCD.
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PMID:Splenectomy in the management of systemic mast cell disease. 240 52

We recently reported that a cloned murine cell line with "natural killer (NK)-like" cytolytic function and prominent cytoplasmic granules also expressed large numbers of plasma membrane receptors (Fc epsilon R) which bound mouse immunoglobulin E (IgE) with high affinity (S.J. Galli et al., 1982, Nature (London) 298, 288). We have now performed IgE-binding studies with 31 additional cloned murine cell lines exhibiting "NK-like" lytic activity (defined as the ability to kill YAC-1 lymphoma cells) and three antigen-specific cytotoxic-T-cell clones. One of the NK-like clones expressed a small number of Fc epsilon R (3.0 X 10(4)/cell) on one of the two occasions it was tested. None of the other clones, which were derived by several different approaches and which had a variety of surface glycoprotein phenotypes, expressed any detectable specific binding of mouse IgE. By contrast, mast cell clones consistently expressed large numbers of Fc epsilon R. The expression of large numbers of high-affinity Fc epsilon R would appear to represent a very uncommon characteristic of NK-like murine cell lines isolated under conditions similar to those described in this report.
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PMID:Lack of detectable immunoglobulin E receptor expression on 33 of 34 cell lines with natural killer-like or cytotoxic-T-lymphocyte activity. 242 20


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