Alteration of mast cell proliferation/apoptosis and expression of stem cell factor in the regression of mastocytoma – report of a case and a serial immunohistochemical study

Inoue, Takato; Yoneda, Kozo; Kakurai, Maki; Fujita, Sachiko; Manabe, Motomu; Demitsu, Toshio

doi:10.1034/j.1600-0560.2002.290509.x

Cited by 6 publications

(4 citation statements)

References 43 publications

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“…24 Spontaneous regression of solitary cutaneous mastocytomas has been shown to be related to apoptosis. 25 Programmed cell death is also involved in spontaneous regression and differentiation of neuroblastomas and may be related to expression of a variety of cell death-related proteases. 26 Spontaneous regression of some neuroblastomas is associated with a form of Ras-mediated programmed cell death that is caspase cascade-independent (non-apoptotic).…”

mentioning

confidence: 99%

Mechanisms of Regression

Elston¹

2004

Clinical Medicine & Research

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mentioning

confidence: 99%

Mechanisms of Regression

Elston¹

2004

Clinical Medicine & Research

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“…Apoptosis has been described as an essential host defence mechanism in order to prevent spreading of infections and to eliminate unwanted cells during tumour growth [31,32]. Some groups have reported caspase-3 and -8-mediated apoptosis in human mast cells in vitro or in mastocytoma and in various inflammatory and fibrotic diseases as liver fibrosis, Crohn's and chronic graft-versus-host-disease [31,33,34]. Based on their in-vitro investigations of human mast cell lines, Berent-Moaz et al (2006) proposed that the extrinsic apoptotic pathway, mediated by the death receptor TRAIL-R (tumor necrosis factor-related apoptosis-inducing ligand) and resulting in caspase-3 activation, might be a mechanism of regulating mast cell survival in vivo and, potentially, for downregulating or resolving mast cell hyperplasia in diseases [35].…”

Section: Discussionmentioning

confidence: 99%

Localization of Active Caspase-3 and Caspase-8 in Nasal Polyps and Nasal Hyperplasia in Consideration of Mast Cell Function: A Semiquantitatively Analysis

Franzke¹,

Koehler²,

Middel³

et al. 2012

IJOHNS

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Introduction:The pathogenesis of nasal polyposis and nasal hyperplasia is still unknown. The localization of caspases in nasal polyps and nasal hyperplasia of patients with and without allergic rhinitis was studied. Methods: Sections of human nasal polyps (n = 5) and hyperplastic nasal turbinates (5 with, 5 without allergy) were stained for active caspase-3 and caspase-8. Double immunofluorescence was used to evaluate colocalization of the caspases with Ki-M1P and tryptase. TUNEL was performed. Results: Active caspase-3 and caspase-8 were seen in nearly all nasal polyps and hyperplastic nasal turbinates. Active caspase-3 was predominantly localized in stromal cells, identified as mast cells. Caspase-8 was localized in mast cells with the pattern similar to active caspase-3 and additionally found in epithelial cells at the nasal and polyp surface and in epithelial cells of glands. Conclusion: Our results suggest that mast cell apoptosis may be involved in the pathological mechanisms which characterize and sustain chronic inflammatory disorders of the nasal mucosa with and without allergy.

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“…On the other hand, monocytes also have a characteristic of mast cells in that they express histamine and histidine decarboxylase (21). Pediatric mastocytoma tends to regress spontaneously at least through the mast cell apoptotic process (22). Our findings of a few foam cells at an early stage, large numbers of foam cells at a later stage, and clinically spontaneous resolution could be explained by the fact that both mast cells and monocytes/macrophages are derived from a common cell origin.…”

Section: Discussionmentioning

confidence: 99%

Plane Xanthoma Associated with Multiple Mastocytoma

Matsumoto

Ikeda

Takeya

et al. 2007

Pediatric Dermatology

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A 5-month-old boy was noted to have brown macules with palpable infiltration on the head, trunk, and extremities a few weeks after birth, with recurrent episodes of generalized flushing and blistering in some of the macules. These lesions developed into yellowish plaques after 1 year of topical treatment with clobetasol propionate. Serum lipid levels were within normal limits. The appearance of the yellowish lesions was similar to that of the xanthelasmoid type of cutaneous mastocytosis. The brown macules showed infiltration of a large number of mast cells and a small number of scattered foam cells, whereas in the yellowish plaques, the number of foam cells was greatly increased. The yellowish plaques regressed spontaneously within a year after cessation of topical corticosteroid treatment. Immunohistochemical analysis found that the foam cells were stained with monocyte/macrophage markers including HAM56, and with SRA-C6, a monoclonal antibody to macrophage scavenger receptor class A (CD204). Therefore, the yellowish plaques were considered to be plane xanthoma associated with cutaneous mastocytoma.

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Alteration of mast cell proliferation/apoptosis and expression of stem cell factor in the regression of mastocytoma – report of a case and a serial immunohistochemical study

Abstract: Loss of MC proliferating activity, an increase in apoptotic MCs, and increased expression of SCF in remaining MCs in RS may play a role in the involution of mastocytomas.

Cited by 6 publications

References 43 publications

Mechanisms of Regression

Mechanisms of Regression

Localization of Active Caspase-3 and Caspase-8 in Nasal Polyps and Nasal Hyperplasia in Consideration of Mast Cell Function: A Semiquantitatively Analysis

Plane Xanthoma Associated with Multiple Mastocytoma

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