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)

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.
J Cancer Res Clin Oncol 1986
PMID:Frequency distribution of tissue mast cells and eosinophilic granulocytes in tumor-draining axillary and paracolic lymph nodes. 377 24

Sixty-four patients with lymphoid lesions involving the lung were separated into three groups. In 32 patients, the predominant lymphoid cell population consisted of small, mature-appearing round lymphocytes with or without plasmacytoid features. This group, designated small lymphocytic proliferation (SLP), represents a heterogeneous group of pulmonary lymphocytic lesions including small lymphocytic lymphoma, lymphocytic interstitial pneumonia, and lymphoid hyperplasia (pseudolymphoma). Thirteen SLP patients were identified as having small lymphocytic lymphoma on the basis of monoclonality, progressive disease in other sites, or both. This group was morphologically identical to the remainder of the SLP patients, except for a higher incidence of plasmacytoid features (P = 0.003) and a greater degree of mast cell infiltration (P less than 0.05). Four of these 13 patients subsequently developed an aggressive large cell lymphoma resulting in death in three patients. The median survival for all of the SLP patients has not yet been reached. Patients in whom a monoclonal cell population could be established showed a slightly worse prognosis of borderline statistical significance (P = 0.09); however, the presence of a serum monoclonal gammopathy conveyed a significantly worse prognosis (P = 0.003). The remaining two groups of patients had various forms of malignant lymphoma other than the small lymphocytic type. One group of 12 patients, designated as having presumed primary lymphoma limited to one or both lungs (PL), had a prolonged course with a median survival of 117 months. The remaining 20 patients had disseminated lymphoma also involving lung (DL); DL patients had a shorter median survival of 33 months.
Cancer 1985 Aug 01
PMID:Pulmonary lymphomas and other pulmonary lymphoid lesions. A clinicopathologic and immunologic study of 64 patients. 383 61

The influence of mast cells on tumor incidence and growth rate was studied in 2 grafted tumor models (fibrosarcoma MC-B6-1 and the Lewis lung carcinoma 3LL). Three kinds of WBB6F1 mice (a cross between WB/ReJ-W/+ and C57BL/6J-WV/+ mice) were used: W/WV (deeply mast cell depleted), WV/+ (partially mast cell depleted), and +/+ (normal mast cell number). The presumed resistance of F1 hybrids to tumor cells of parental origin was observed in 12 of 13 +/+ mice, but only in 11 of 22 WV/+ mice and in none of 39 W/WV mice. Tumor incidence and metastasis incidence were inversely correlated with tissue histamine levels and mast cell number. Growth rates of tumors were similar in W/WV and WV/+ mice, but the tumor growth rate was much slower in the only +/+ mouse in which the tumor grew. These results confirm the protective role of mast cells against tumors.
J Natl Cancer Inst 1985 Mar
PMID:Inverse correlation between tumor incidence and tissue histamine levels in W/WV, WV/+, and +/+ mice. 385 69

The epidermal and dermal effects of protracted 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment (2 micrograms TPA twice weekly) of Sencar mouse skin were studied using cell kinetics and morphometric techniques. In addition, regression of TPA-induced changes was evaluated after cessation of 56 topical applications. During the first week of treatment a reactional hyperplasia, characterized by cell damage, edema, and acute inflammation in both epidermis and dermis, occurred. This picture changed gradually during the following 3 weeks: an epidermal hyperplasia devoid of involutional or inflammatory features was accompanied by a moderate to mild chronic inflammation of the dermis and a hyperplasia of the hair follicles. This remained throughout the experimental period until the topical TPA treatment ceased. Although TPA induced papillomas in only 5% of the animals (maximum = 2 papillomas/animal and no carcinomas), all sustained marked epidermal hyperplasia of approximately 4 to 5 times the normal thickness, and increased the number and volume of hair follicles. The [3H]thymidine pulse-labeling index of the basal layer was approximately 32% (normal congruent to 6%). The level of dark keratinocytes remained constant; i.e., 8% of the basal cells were identified as dark cells during the entire experiment. At the subepidermal level the dermal thickness and total cellularity increased, although the proportion of the different cell types changed during the treatment. The mast cell population increased remarkably. After TPA treatment ceased, most of these parameters regressed abruptly during the first 2 weeks. Two to 4 months later, the epidermis was slightly thinner, and the labeling index was 50% lower than normal (2.8%). This study shows that prolonged repetitive TPA applications induced a steady-state hyperplasia without tachyphylaxis, and that this alteration regressed rapidly after treatment ceased. In addition, labeling-index values lower than normal were reached soon after normalization, suggesting that a possible selection of keratinocytes, dependent on TPA for proliferation, took place during the chronic administration of topical TPA. The number of hair follicle, capillary vessels, mast cells, and the dermal thickness never reached normal values after treatment. These important changes in the dermis and hair follicles indicate that the target cells for tumor promoters are not confined to the epidermis alone, and that these tissues could participate actively in carcinogenesis directly, either as tumor-originating tissues (hair follicles), or as inducers or helpers of neoplastic growth (connective tissue cells).
Cancer Res 1985 Jun
PMID:Cutaneous changes during prolonged application of 12-O-tetradecanoylphorbol-13-acetate on mouse skin and residual effects after cessation of treatment. 398 7

Surface membrane antigen(s) expressed on a mouse mast cell line (FMP1) have also been shown to occur on hemopoietic spleen colony-forming units (CFU-S) and granulocyte/macrophage colony- and erythroid burst-forming cells, using a xeno-antiserum raised against FMP1 cells. This mast cell model has been used to obtain antiserum and large quantities of antigen for the biochemical identification of CFU-S and progenitor cell antigen(s). Immunoprecipitation of FMP1 membrane antigens with the antiserum and subsequent polyacrylamide gel electrophoresis revealed the presence of five membrane proteins with molecular weights of 28,000, 32,000, 36,000, 50,000, and 70,000. Mouse B-lymphoma cell line W279 which reacted with anti-FMP1 serum was found to possess three immunoprecipitable surface proteins with molecular weights of 32,000, 50,000, and 70,000. Attempts have been made to identify the antigen(s) expressed by CFU-S and progenitors which were revealed by immunoprecipitation from the tumor lines. The three lower-molecular-weight proteins (Mr 28,000-36,000) were chosen for initial study. Membrane extracts of FMP1 cells were fractionated on Sephacryl S-200, and selective pools of these antigens were made. Antisera to these pools exhibited complement-dependent cytotoxicity to FMP1 cells, bone marrow CFU-S, granulocyte/macrophage colony-forming cells, and erythroid burst-forming units. These antisera immunoprecipitated Mr 28,000, 32,000, and 36,000 proteins from FMP1 cell membrane extracts but not the Mr 50,000 and 70,000 antigens. The W279 line has only one antigen (Mr 32,000) in the lower-molecular-weight range and is able to absorb anti-CFU-S and anti-progenitor activity, which suggests that it is this antigen which is expressed on hemopoietic cells. In addition, thymocytes react with anti-FMP1 serum, and the Mr 32,000 antigen was immunoprecipitated from thymus cell extracts. Binding studies with concanavalin A, wheat germ agglutinin, and lentil lectin indicated that the Mr 28,000-36,000 proteins were glycoproteins. The apparent molecular weights of these proteins on polyacrylamide gels were not altered by reduction and alkylation and therefore do not contain disulfide-linked subunits.
Cancer Res 1985 Oct
PMID:Identification of a tumor cell-derived differentiation antigen on mouse colony-forming units in the spleen and progenitor cells. 402 83

Systemic mast cells disease (SMCD) is an uncommon disorder that constitutes approximately 10% of all mastocytoses. Diagnosis requires a substantial degree of clinical suspicion, which may not be present if characteristic skin lesions of urticaria pigmentosa are not observed. Lack of well-defined histopathologic features for the disease have delayed or prevented the diagnosis of SMCD. An initial diagnosis of "myeloproliferative disorder," chronic granulocytic leukemia, or myelofibrosis is frequently made. Study of the clinical and pathologic features of 26 cases of SMCD indicated that affected patients are generally middle aged and may have had urticaria pigmentosa for many years. Gastrointestinal symptoms are common, and splenomegaly and hepatomegaly along with radiographic evidence of generalized bone disease are usually noted. Hematologic factors are highly variable. Characteristic histopathologic features of SMCD are described for bone marrow, lymph nodes, liver, and spleen. The authors consider tissue fixation and staining methods to help identify mast cell lesions.
Cancer 1982 Mar 01
PMID:Systemic mast cell disease: a clinical and hematopathologic study of 26 cases. 617 98

Using a pH-adjusted toluidine blue stain (pH range, 2.5-6.5), we sequentially examined the staining patterns of mast cells in tissue sections taken from patients with localized or reactive mast cell lesions and benign or malignant mastocytosis syndromes. Reactive or benign lesions stained well over the entire range of pHs and were separated from malignant mast cell proliferations which stained poorly and with greatest intensity in the less acidic range (pH greater than 3.5). Patients with disseminated mast cell lesions but without tumor masses or leukemia had a staining pattern between that of benign and malignant lesions. Basophils stained intensely at pH 2.5, and metachromasia rapidly diminished at higher pH. The use of the pH dependent toluidine blue stain may be an adjunct in recognizing patients with mast cell lesions, predicting their prognosis, and distinguishing basophils from mast cells.
Cancer 1983 Mar 15
PMID:Benign and malignant mast cell proliferations. Diagnosis and separation using a pH-dependent toluidine blue stain in tissue section. 618 13

The effect of infection with Moloney murine leukemia virus (Mo-MuLV) on long-term bone marrow cultures was studied. Cultures were derived from the bone marrow of BALB/Mo mice, which carry Mo-MuLV as an endogenous virus, or from BALB/c, 129/J, or balb/c X 129/J mice that were infected with Mo-MuLV in vitro. The following parameters were tested: longevity of generation of granulocytes; biological properties of nonadherent cells in colony-forming assays for pluripotential stem cells and committed granulocyte-macrophage colony-forming unit culture, erythroid, or metachromasia-positive mast cell-basophil colony-forming cells; differentiation of nonadherent cells following cocultivation with thymic or bone marrow stromal cells; and generation of WEHI-3 dialyzed conditioned medium-dependent permanent cell lines. Granulocytes were generated for 65 weeks in BALB/Mo marrow cultures, 31 weeks for BALB/c, 22 weeks in 129/J, and 28 weeks in balb/c X 129/J cultures. Exogenous infection of BALB/c cultures with Mo-MuLV increased the longevity of hematopoiesis to 41 weeks. Granulocyte-macrophage colony-forming unit cultures were produced for 61 weeks in BALB/Mo cultures, 25 to 40 weeks in Mo-MuLV-infected cultures, and 19 to 33 weeks in uninfected control cultures. Nonadherent cells harvested from BALB/Mo marrow cultures generated cloned permanent WEHI-3 dialyzed conditioned medium-dependent, nonleukemogenic granulocyte-macrophage colony-forming unit culture cell lines at greater efficiency than did Mo-MuLV-infected or uninfected BALB/c cultures. The cell lines differentiated to mature granulocytes following cocultivation with purified marrow or thymic stromal cells. There was no detectable differentiation of nonadherent cells to lymphocytes or mast cells. Thus, Mo-MuLV does not detectably transform granulocyte progenitor cells in vitro to granulocytic leukemia. However, Mo-MuLV replication stimulates self-renewal of granulocyte progenitor cells in both primary marrow culture and in suspension culture in WEHI-3 dialyzed conditioned medium.
Cancer Res 1981 Sep
PMID:Effects of murine leukemia virus infection on long-term hematopoiesis in vitro emphasized by increased survival of bone marrow cultures derived from BALB/Mo mice. 626 58

Peritoneal macrophages from BD IX rats collected 24 hr after an i.p. injection of ADriamycin (10 mg/kg) were cytotoxic to syngeneic cancer cells in culture. In contrast, incubation in vitro in Adriamycin solutions did not evoke tumoricidal activity in peritoneal macrophages, whatever the incubation time (from 1 to 24 hr) and the Adriamycin concentration (from 1 ng to 100 micrograms/ml). Macrophages incubated with Adriamycin in vitro accumulated the drug in their nuclei, whereas macrophages from animals receiving Adriamycin in vivo accumulated it is cytoplasmic vacuoles. Early observation of peritoneal cells after in vivo exposure to Adriamycin shows that Adriamycin is concentrated in mast cell granules which are released and then phagocytosed by peritoneal macrophages. Mast cells exposed to Adriamycin in vitro can induce macrophages to become cytotoxic. These facts explain the difference between macrophages exposed to Adriamycin in vivo and in vitro. Adriamycin fluorescence appears in nuclei of cancer cells incubated with in vivo-labeled macrophages, suggesting that macrophages can directly transfer the drug into cancer cells and therefore play a role in the Adriamycin antitumor effect.
Cancer Res 1982 Sep
PMID:Tumoricidal effect of macrophages exposed to adriamycin in vivo or in vitro. 628 14

Six patients exhibiting severe pancytopenia or overt leukemia associated with myelofibrosis after chemotherapy for malignant disease have been investigated by immunologic techniques and ultrastructural cytochemistry. Initially, five patients displayed severe thrombocytopenia contrasting with mild neutropenia and anemia. Bone marrow biopsies showed a clear megakaryocytic proliferation and an excess of immature mononuclear cells. The demonstration of peroxidase activities at the ultrastructural level and immunofluorescence labeling with a panel of monoclonal antibodies, including an antiplatelet glycoprotein Ib and an antiglycoprotein IIb-IIIa complex, on blood or marrow cells, permitted identification of otherwise unidentifiable promegakaryoblastic proliferation. In two patients, the use of an immunoperoxidase technique with an antifactor VIII-R-Ag antibody has allowed direct confirmation of this diagnosis on bone marrow sections. This megakaryoblastic proliferation was not pure and was variably associated with blasts of other cell lines (erythroblasts or myeloblasts). Changes in the population of blasts were observed during evolution in two patients. The sixth patient had a mild thrombocytopenia associated with severe neutropenia and anemia. Bone marrow biopsy displayed a myelofibrosis and immature cells, without megakaryocytic proliferation. Ultrastructural study revealed a pure basophil-mast cell proliferation. In conclusion, in five of six patients with secondary acute leukemia associated with myelofibrosis, a proliferation of promegakaryoblasts was demonstrated using both immunofluorescent and ultrastructural cytochemical techniques.
Cancer 1984 Oct 01
PMID:Therapy-related leukemia associated with myelofibrosis. Blast cell characterization in six cases. 638 Jul 2


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