Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10721 (c-kit)
 6,575 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pericryptal fibroblasts (PFs), a class of myofibroblasts, have strongly been implicated in the regulation of villous structure because of their location close to crypts and their ability to secrete cytokines affecting intestinal epithelial cell proliferation and differentiation. Recently, mast cells (MCs) have also been involved in the homeostasis of villous architecture. As myofibroblasts arise in a wide variety of settings concurrently with a local increase in the number of tissue MCs, we calculated in this study the density of both PF and distinct pericryptal MC phenotypes in the mucosa of human duodenum showing normal, defective, or atrophic villous profiles. In addition, we evaluated the statistical association between PF-MC densities and each pattern of villous architecture. Finally, we correlated the density of PF with the density of pericryptal MC phenotypes. For this purpose, samples taken by endoscopy from 30 patients complaining of inflammatory bowel disorders were studied by immunohistochemistry. The densities of alpha-smooth muscle actin-positive PFs as well as tryptase-, chymase-, and c-kit-positive MCs were determined in the crypt lamina propria. Villous architecture was found to be significantly associated with the number of PFs and tryptase-, chymase-, c-kit-positive MCs in the lamina propria (ANOVA group effect P < 0.001). High density of both PFs and MCs was found in intestinal samples with normal villous morphology while lower densities were associated with defective or atrophic villous profiles (Tukey's test for multiple comparison P < 0.001). In addition, a significant correlation was found between PF density and the density of each pericryptal MC phenotype (vs. tryptase-positive MCs, r = 0.913; vs. chymase-positive MC, r = 0.905; vs. c-kit-positive MC, r = 0.927; P < 0.001 in all cases). This study provides morphological support for an important cooperation between PFs and MCs in maintaining normal villous architecture.
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PMID:Number of pericryptal fibroblasts correlates with density of distinct mast cell phenotypes in the crypt lamina propria of human duodenum: implications for the homeostasis of villous architecture. 1665 53

Among the intestinal tumors of hematopoietic cell origin, lymphoma is the most common in the dog. Herein, we characterized the clinical and pathologic features of 11 dogs (average age, 10.6 +/- 2.5 years) with T-cell lymphoma of the intestinal tract with eosinophil infiltrates. No sex predominance was apparent. All had localized tumor masses in the small intestine. Grossly, the intestinal wall was thickened, and the lumen of the affected intestine was usually narrowed. Microscopically, we observed transmural diffuse invasion of round to pleomorphic tumor cells. Tumor cells showed varying morphology, from scanty to abundant cytoplasm, and round to ovoid nuclei with scattered to dense chromatin. In seven of the dogs, tumor cells had infiltrated into the epithelium. All showed infiltration of eosinophils and all 11 tumors had a T-cell phenotype (CD3+, CD79-). Only one tumor stained positive for the mast cell marker c-kit and none was positive for mast cell tryptase. We did not observe ultrastructurally apparent granules in any of the tumor cells. These results suggest that, in dogs, T-cell lymphomas of intestinal origin resemble mast cell tumors of intestinal origin with respect to cell structure and eosinophil infiltration. Therefore, in the absence of epitheliotropism, it is difficult to confirm the differential diagnosis without immunostaining for mast cell and lymphocyte markers, including mast cell tryptase, c-kit, CD3, and CD79.
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PMID:T-cell lymphoma with eosinophilic infiltration involving the intestinal tract in 11 dogs. 1667 80

A 46-year-old woman was admitted to the hospital with complaints of chronic diarrhoea, vomiting and severe muscle weakness. Clinical examination showed a lethargic, malnourished, dehydrated patient with ascites and bilateral leg oedema. Laboratory evaluation revealed mild normochromic normocytic anaemia and severe hypoproteinaemia with hypoalbuminaemia. Upper gastrointestinal endoscopy showed a thickened, friable duodenal mucosa with multiple erosions. Colonoscopy revealed nodular, pseudopolypoid lesions with patchy erosions in the left hemicolon. Haematoxylin-eosin stained sections from biopsies of endoscopically abnormal bowel segments showed multi-focal aggregates of large, histiocyte-like cells with abundant pale cytoplasm in the lamina propria. These cells were negative on PAS, Ziehl-Neelsen, Giemsa and toluidine blue stains. Their immunophenotype was CD68 (+), c-kit/CD117 (+) and mast cell tryptase (+), which is consistent with mast cells. A trephine biopsy showed diffuse replacement of the bone marrow by atypical, monomorphic, frequently spindle-shaped mast cells. No associated haematopoietic malignancy was detected. The final diagnosis was aggressive systemic mastocytosis with involvement of the gastrointestinal tract complicated by protein-losing enteropathy. This association has not been reported previously. The patient has been treated with prednisolone and interferon-alpha and has since recovered.
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PMID:Aggressive systemic mastocytosis complicated by protein-losing enteropathy. 1684 41

It is becoming accepted that multiple cell types in stromal microenvironment are involved in tumorigenesis. In this setting, mast cells (MC) display a diversity of roles that may contribute to the defense against tumors or tumor progression. Thus, the aim of this study was to evaluate density and migration of MCs in OSCC (oral squamous cell carcinoma) and pre-malignant oral hyperkeratosis (leukoplakia) as well as their relationship with clinical and microscopic parameters. The tryptase and c-kit expression was analyzed in 38 cases of OSCC, 26 cases of leukoplakia, and 12 cases of clinically healthy oral mucosa (control) by means of immunohistochemistry. The tryptase(+) cell numbers were decreased in OSCC (P=0.0003) and leukoplakia (P=0.03) compared with control. Similar numbers of tryptase(+) cells were observed in leukoplakia and OSCC (P=0.31). The density of c-kit(+) MCs was also significantly lower in OSCC and leukoplakia in relation to control resulting in a reduced c-kit(+)/tryptase(+) relationship in OSCC (19%) in comparison with leukoplakia (59%) and control (63%). No correlation was observed between MC populations with clinical and microscopic characteristics of OSCC. Our findings suggest that the decrease in MC numbers in pre-malignant and malignant oral lesions may be related to the migration failure of these cells, possibly reflecting an important modification in the microenvironment during tumor initiation and progression.
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PMID:Decrease in mast cells in oral squamous cell carcinoma: possible failure in the migration of these cells. 1697 74

Mast cells (MCs) are important effector cells in mucosal defense and allergic inflammation. Lymphoid tissues such as tonsils and adenoids also have modest numbers of MCs. However, the role of MCs in lymphoid tissues is not well known. In this study, we showed the local distribution of MCs in tonsils from IgE-mediated allergic or nonallergic donors, studied their ultrastructure, and specified their surrounding cell types. Tonsils were obtained from IgE-mediated allergic or nonallergic donors suffering from chronic tonsillitis or hyperplastic tonsils. The localization and distribution of MCs and IgE binding to MCs were determined by immunohistochemistry using antibodies against tryptase, c-kit, and IgE. In addition, mast cell structure was examined using electron microscopy. In both allergic and nonallergic donors, MCs were distributed mainly in the interfollicular area and the perivascular area of connective tissue. We found that the total number of MCs in tonsils was almost the same in both donor groups. However, the number of MCs in the interfollicular area was significantly higher in nonallergic versus allergic donors. Moreover, the electron microscopy revealed that MCs localized in perivascular areas of connective tissue have scroll-type granules, and MCs in the interfollicular areas contained both particle and scroll-type granules. In addition, the MCs that were surrounded by CD4+ lymphocytes in the interfollicular area showed empty granules, whereas MCs in the perivascular area, not surround by CD4+, were intact. This implies that these MCs were degranulated, and this probably was caused by CD4+ cells. Taken together, these findings suggest that tonsillar MCs distribute differently in allergic and nonallergic donors, and that MCs in the interfollicular area might be activated by direct contact with CD4+ T cells.
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PMID:Comparison of human tonsillar mast cell localization and ultrastructural observations between IgE-mediated allergic and nonallergic donors. 1706 73

A 41-year-old woman presented with a 2-month history of pruritus and a generalized dermatitis that developed initially on the head and spread to the trunk, legs, and buttocks. The pruritus caused extreme discomfort and was not relieved by antihistamines or topical steroid treatment. The patient denied flushing, syncope, and vomiting. Her medical history included asthma treated with salmeterol/fluticasone propionate inhaler, and status post silicone breast augmentation. Physical examination revealed a papular dermatitis on the trunk and extremities composed of lesions up to 0.5 cm in diameter, surrounded by excoriation marks (Figure 1). There was no hepatosplenomegaly or lymphadenopathy. Darier's sign was negative. Results of complete blood count, peripheral blood film examination, and liver function tests were all with normal limits. A biopsy specimen taken from a lesion and stained with hematoxylin-eosin showed telangiectasias, with an increased number of mast cells around blood vessels (Figure 2). Positive Giemsa (Figure 3) and c-kit stain (Figure 4) indicated an increased number of mast cells. Bone marrow aspiration and total body CT performed to rule out systemic involvement showed no pathology. Protein electrophoresis was normal. Serum tryptase and histamine were within normal limits, and 24-hour urine collection for histamine was normal. Narrow-band UV-B treatment was begun 3 times weekly, reduced to twice weekly after 2 months, and then stopped. The first few treatments resulted in significant relief of the pruritus and regression of lesions. After 3 months without treatment, the patient remained free of pruritus and lesions.
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PMID:Telangiectasia macularis eruptiva perstans: unusual presentation and treatment. 1708

We retrospectively analyzed the clinical relevance of hydrodistention under anesthesia for patients having urgency and/or lower abdominal pain who were clinically diagnosed as having interstitial cystitis (IC) from May 1996 to May 2005. Their symptoms were refractory to anticholinergic or antiinflammatory agents. Hydrodistention was performed under general or spinal anesthesia with direct vision by cystoscopy and irrigation fluid was instilled into the bladder at a pressure of 80 cmH2O. Cystoscopic findings revealed glomerulation in 26 patients (96%), cracking in 10 (37%) and Hunner's ulcer in 3. Twenty-four patients (89%) obtained improvement of the objective symptoms after treatment. However, symptoms soon deteriorated in 16 patients, and the average duration of efficacy was only 4.7 months (SD; +/-3.7). There were two episodes of complication in this treatment. Bladder rupture occurred during hydrodistention, but was successfully managed with simple percutaneous perivesical drainage. One patient with acute pyelonephritis was treated with an antimicrobial agent without any additional treatment. Although bladder specimens were examined by immunohistochemistry, tryptase and c-kit were not linked with the mast cell count, severity of symptoms or treatment efficacy. Hydrodistention of the bladder may be recommended as the first treatment choice for patients with IC because it provides relatively high efficacy. However, the short duration of the efficacy requires a second-line treatment option for better management of patients with IC.
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PMID:[Hydrodistention of the bladder in patients with interstitial cystitis--clinical efficacy and its association with immunohistochemical findings for bladder tissues]. 1713 63

The mast-cell sarcoma of a bone is described here for the first time. The tumour presented in a 4-year-old boy, with pain, oedema and deformation of his right lower leg. Radiological findings revealed a destructive tumourous mass. Histopathological examination showed the tumour to be composed of large, atypical cells, with hyperchromatic oval and polygonal nuclei. The cytoplasm around them was eosinophilic with many basophilic and toluidine-blue-positive granules. These atypical mast cells were positive for chloroacetate esterase, c-kit, tryptase and negative for myeloperoxidase. The primary disease quickly progressed to mast-cell leukaemia, and despite intensive chemotherapy the patient died 18 months after first symptoms.
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PMID:Mast-cell sarcoma of the tibia. 2177 98

Mast cells are known to be involved in type I allergy and to be localized in almost all tissues in the body. However, they have slightly different properties depending on their tissue of residence. Although mast cells are found in skeletal muscle tissue, there have been no reports of their appearance in cultured skeletal muscles. We report here that mast cells appear in long-term cultures of skeletal muscles from neonatal rats and rat fetuses. When muscle cells were disseminated and cultured in minimum essential medium with 10% fetal calf serum and 10% horse serum, oval cells containing large granules started to appear on myotube sheets at 5 days of culture. These oval cells continued to proliferate for 2-3 months, and showed immunoreactivity for histamine, tryptase, Fc(epsilon)RI, and c-kit. They showed metachromatic staining with 0.5% toluidine blue at pH 0.5 and were stained with both Alcian blue and safranin. Biochemically measured histamine content per dish was significantly higher in 2-month than in 5-day culture. From these results, we concluded that these oval cells were mast cells. Because proteases from mast cells have been reported previously to affect myoblast proliferation, the present findings suggest that there may be some interaction between mast cells and muscle cell proliferation or differentiation. The present finding that mast cells are easily obtained from ordinary skeletal muscle cultures provides a useful method for the study of the diverse functions of mast cells.
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PMID:Mast cells appearing in long-term skeletal muscle cell cultures of rat. 1785 3

Systemic mastocytosis (SM) is characterized by the accumulation of neoplastic mast cells in bone marrow and other organs. Gastrointestinal (GI) symptoms are common in both SM and cutaneous mastocytosis [urticaria pigmentosa (UP)], and are usually caused by the release of histamine and other inflammatory mediators. Occasionally, neoplastic mast cells may also directly infiltrate the GI tract. Previous studies have suggested that enumeration of the mast cells in GI biopsies may help establish the diagnosis of SM. However, mast cells have been reported to be increased in various inflammatory diseases, and mast cell density has not been systematically evaluated in other GI disorders. Recently, expression of CD25 by mast cells in bone marrow has been shown to be specific for SM. The purpose of this study was (1) to quantitate and compare mast cells in mucosal biopsies from patients with SM involving the GI tract, UP with GI symptoms, and a control group of diverse inflammatory disorders, and (2) to determine whether immunostaining for CD25 can be used to distinguish neoplastic from reactive mast cells in GI biopsies. Seventeen GI biopsies from 6 patients with SM; 17 GI biopsies from 5 patients with UP; and 157 control cases including 10 each normal stomach, duodenum, terminal ileum, and colon, Helicobacter pylori gastritis, bile reflux gastropathy, peptic duodenitis, celiac disease, Crohn disease, ulcerative colitis, lymphocytic colitis, and collagenous colitis, 20 biopsies from 16 patients with irritable bowel syndrome, 8 biopsies from 5 patients with parasitic infections, and 9 biopsies from 7 patients with eosinophilic gastroenteritis were immunostained for mast cell tryptase, c-kit (CD117), and CD25. Mucosal mast cells were quantitated, and the presence or absence of CD25 expression on mast cells was determined. In SM patients, mast cells in the small intestine and colon numbered >100/high-power field (HPF) in nearly all cases (mean 196/HPF; range 74 to 339). This was significantly higher than in GI biopsies from UP patients (mean 17/HPF; range 8 to 32, P<0.0001) and all inflammatory diseases (P<0.01). Mast cell density in other disorders ranged from a mean of 12/HPF in H. pylori gastritis to 47/HPF in parasitic infections. Interestingly, all SM biopsies (and none of the other cases) contained aggregates or confluent sheets of mast cells. In addition, mast cells in all SM cases were positive for CD25, whereas GI mucosal mast cells in UP and all other control cases were negative. In conclusion, quantitation of mast cells can be helpful to diagnose SM in GI mucosal biopsies, although mast cells are also markedly increased in parasitic infections. Aggregates or sheets of mast cells are only seen in SM. Immunoreactivity for CD25 in GI mucosal mast cells is specific for SM and can be used to confirm the diagnosis.
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PMID:Immunoreactivity for CD25 in gastrointestinal mucosal mast cells is specific for systemic mastocytosis. 1805 23


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