PubMed · 14038080
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J B WOHLGEMUTH. 1962-03-09. [Giant cells].. https://doi.org/10.1055/s-0028-1111782
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Tuberous sclerosis (TSC) is an autosomal dominant disease characterized by the formation of hamartomatous lesions in many organs, including brain, heart or kidneys. It has been found that TSC is caused by the mutation in one of the two tumor suppressor genes: TSC1 or TSC2, encoding hamartin and tuberin, respectively. According to Knudson's two-hit model of tumorigenesis, second-hit mutation and resulting loss of heterozygosity (LOH) of a tumor suppressor gene is necessary for tumor formation. In fact, LOH is commonly found in several types of hamartomas formed in the process of tuberous sclerosis, but, interestingly, not in brain lesions, containing characteristic giant cells. In this paper, we review literature covering origination of giant cells and present several hypotheses explaining why in spite of the presence of hamartin and tuberin, brain lesions form in TSC patients.
Cells with significantly enlarged nuclei have been described in basal cell carcinomas, dermatofibromas, and pleomorphic fibromas, to name a few. These cells are typically visible using low power microscopy and have been termed "pleomorphic" or "monster cells." They have not been previously described in cutaneous melanomas. We sought to determine the prevalence of monster cells in otherwise conventional biopsies of primary cutaneous melanomas and its association with other histopathologic features of this malignancy. Ninety-nine superficial spreading melanomas, nodular melanomas, and acral lentiginous melanomas/lentigo malignas were retrospectively evaluated for the presence of monster cells, multinucleated giant cells, ulceration, inflammation, and depth of invasion (Breslow level). Thirteen cases of melanoma containing monster cells were found. A statistically significant association was noted between the presence of these cells, the histologic subtype of nodular melanoma (P = 0.0125), ulceration (P = 0.0127), the depth of invasion (P = 0.0103), and the presence of multinucleated giant cells (P = 0.0016). The finding of monster cells is not an uncommon occurrence and is seen more often in nodular melanomas.
OBJECTIVE: To detect the expression of RANKL and OPG protein in the giant cell lesions of jaw and to study the mechanism of this lesion. METHODS: RANKL and OPG were detected by immunohistochemistry (SP) in 24 paraffin-embedded and 2 frozen specimens of central giant cell lesion of jaw. RESULTS: RANKL signals were strongly positive in the vascular epithelial cells. They also could be found in fibrous stroma, bone matrix, and stromal spindle cells, even in some cytomembrane of multinucleated giant cells. OPG was detected in multinucleated giant cells and a fraction of round mononuclear cells. CONCLUSIONS: Active vascular epithelial cells are contributed to the formation of multinucleated giant cells through regulating RANKL, and RANKL could play its role by paracrine and autocrine, which might be inhibited by OPG.