Stewart‐Treves syndrome: an histogenetic (ultrastructural and immunohistological) study

Abstract

One case of the so‐called „Stewart‐Treves syndrome” (STS), appearing on a lymphoedomatous arm complicating radical mastectomy for brest cancer, was characterized electronmicroscopically and immunohistologically, in order to elucidate its disputed (epithelial vs endothelial) histogenesis. Epithelial and endothelial differentiation markers used comprised: antibodies against keratin, vimentin, factor VIII‐related antigen (F VIII‐RA), HLA‐DR antigens and the lectin Ulex europeaus agglutinin 1 (UEA I). At the ultrastructural level, neoplastic cells were found to contain typical Weibel‐Palade bodies, whereas by immunohistological techniques they proved to be keratin −negative/vimentin+, F VIII‐RA +, UEAI+, HLA‐DR+. These results rule out a possible epithelial differentiation and strongly favour an endothelial one for STS.

Lymphangiosarcoma in Chronic Lymphoedema

“…It is established by history, clinical examination and light microscopic evaluation of biopsy material. In difficult cases differentiation can be achieved by monoclonal antibodies (Hashimoto et al, 1985;Kanitakis et al, 1986). In our case, monoclonal antibodies (CD31 and EMA) supported the morphological features of the malignant vascular tumour.…”

Angiosarcoma with dermal melanocytosis

“…Light and electron microscopy, lectin histochemistry and immutiohistochemistry confirmed a vascular origin for the neoplastic tumor cells frotn the primary lesion. In addition, both metastatic lesions had histopathology atid ultrastructure typical of atigiosarcoma of the skin (5)(6)(7)(8)(9). The primary lesion cells containing melatiiti-like substatice were identified by electron microscopy and immunohistochemistry as melanocytes, thus confirming a diagnosis of angiosarcoma with dermal melanocytosis.…”

Syndrome de Stewart-Treves (angiosarcome sur lymphœdème) : complication rare du lymphœdème

“…Cependant, l'abondance cytoplasmique en microfilaments est variable, faible pour Pizzi et al (30), réelle pour Unruh et al [31]. Des études récentes suggèrent que l'origine de cellules dans le SST est plutôt endothéliale qu'épithéliale [17,[32][33][34][35][36] La nature vasculaire et conjonctive de ces tumeurs a été confirmée par immunohistochimie, en montrant l'affinité endothéliale pour l'anticorps antifacteur VIII et la positivité pour certains marqueurs de filaments intermédiaires (actine, vimentine) [37]. Aucun marqueur cytogénétique spécifique n'a, jusqu'à présent, été rapporté dans le syndrome de Stewart-Treves.…”