Immunohistochemical demonstration of factor XIIIa expression in neurofibromas. A practical means of differentiating these tumors from neurotized melanocytic nevi and schwannomas

Gray, M. H.

doi:10.1001/archderm.126.4.472

Cited by 18 publications

(9 citation statements)

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“…Data about the dermal dendrocyte's presence in different dermatopathologic states and conclusions about its presumptive role are often conflicting (Nemes and Thomazy 1988;Cerio et al 1988;Nemeth and Penneys 1989;Nickoloff and Griffiths 1989a, b;Cerio et al 1989b;Toida et al 1989;Penneys 1990;Cerio and Jones 1990a, b;Gray et al 1990Gray et al , 1991Penneys et al 1991;Regezi et al 1993;Gibran et al 1994a). Distinction of the dermal dendrocyte from fibroblasts, macrophages, Langerhans cells and other dendritic cells of the immune system has been based on immunocytochemical localization of cell markers.…”

Section: Discussionmentioning

confidence: 99%

Ontogeny and characterization of Factor XIIIa+ cells in developing human skin

1996

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Factor XIIIa (FXIIIa), a coagulation transglutaminase, is a cytoplasmic marker for dermal dendritic cells reported to be bone marrow-derived, phagocytic and antigen-presenting. In non-inflamed skin, these cells populate the papillary dermis in a perivascular distribution. They are increased in dermatoproliferative disorders and have been implicated as dermal stimulants for psoriatic hyperkeratosis. Since developing skin provides an example of dermal influence on the epidermis, we evaluated the presence of FXIIIa+ cells in human fetal skin to determine whether their location would suggest a role in morphogenetic events in the skin. Embryonic and fetal skin of progressive estimated gestational ages (EGA) was examined using immunocytochemistry with a polyclonal antibody to FXIIIa. At 6 weeks EGA, globular FXIIa+ cells were present in the hypodermis. By 7-8 weeks, a compact sub-epidermal network of fusiform FXIIIa+ cells was also evident. By 11-12 weeks, the sub-epidermal cellular network was no longer FXIIIa+, but discrete FXIIIa+ dendritic cells were present in the reticular dermis. With advancing gestational age, FXIIIa+ dendritic cells populated the papillary dermis in a perivascular distribution. This adult-like distribution persisted through 22 weeks EGA, the oldest specimen examined. Because FXIIIa+ cells were evident in embryonic skin before the onset of bone marrow hematopoietic function, the skin was double-labeled with the FXIIIa antibody and with monoclonal antibodies to CD45 (marker for bone marrow-derived cells), CD68 (marker for macrophages) and HLA-DR (class II major histocompatibility antigen). Most of the FXIIIa+ dendritic cells did not colocalize CD45, but were CD68+; some cells did react with the HLA-DR antibody. Notably, the FXIIIa+ cells of the sub-epidermal network in the 7 weeks EGA specimens did not react with the other antibodies. We conclude that FXIIIa+ cells are first present in embryonic hypodermis and sub-epidermal dermis and later they are distributed in the papillary dermis in a perivascular pattern. In embryonic skin FXIIIa+ cells are not exclusively dendritic. Our data support the idea that cells that express FXIIIa do not constitute a unique bone marrow-derived cell type, but that multiple cell types produce FXIIIa.

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Section: Discussionmentioning

confidence: 99%

Ontogeny and characterization of Factor XIIIa+ cells in developing human skin

1996

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“…We have also compared the sensitivity and specificity of the murine antibody MUM1 with anti S100, HMB45, and anti-MelanA. Finally, we have examined the ability of the MUM1 antibody to distinguish nerve sheath proliferations such as schwannomas, neurofibromas, and malignant peripheral nerve sheath tumors (MPNST) from melanocytic proliferations, as nerve sheath lesions are frequently in the differential diagnosis of benign melanocytic lesions and desmoplastic malignant melanoma (20).…”

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confidence: 99%

Expression of the B-Cell Proliferation Marker MUM1 by Melanocytic Lesions and Comparison with S100, gp100 (HMB45), and MelanA

et al. 2003

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The diagnosis of malignant melanoma remains one of the most difficult to render in surgical pathology, partially because of its extreme histologic variability. Limits in the sensitivity and/or specificity of the currently available melanocytic markers such as anti-S100, HMB45, and anti-MelanA further complicate this problem. Previous work has demonstrated that the B-cell proliferation/differentiation marker MUM1/IRF4 is detected in malignant melanoma and hematolymphoid malignancies, but not in any other neoplasm tested (including colonic, lung, breast, and ovarian carcinomas). In the current study, we have examined MUM1 protein expression in 61 melanocytic lesions and compared the diagnostic usefulness of this marker with that of anti-S100, HMB45, and anti-MelanA

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“…18 Neurofibromas are positive for factor XIIIa and negative for CD 56. 20,21 The presence of neurofilament within the tumor would be indicative of neurofibromas as they grow within the nerve of origin in contrast to schwannomas. 14 If the question of malignancy arises in a tumor of this kind, Ki67 would aid the diagnosis as it has a low proliferative fraction in benign lesions.…”

Section: Discussionmentioning

confidence: 99%