PubMed · 5035759
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D R Turner. 1972. Membranous nephropathy.. https://pubmed.ncbi.nlm.nih.gov/5035759/
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Tumor-induced blood vessel formation is a key process for the growth and spread of solid tumors, traditionally attributed to activated host endothelial cells (angiogenesis). Recently, highly aggressive cancer cells have been shown to form vascular channels in the absence of endothelial cells (vasculogenic mimicry). In this work, we have focused on the common dependence of both processes in their interactions with the surrounding extracellular matrix. We had previously described a human recombinant anti-laminin antibody that blocked the capillary morphogenesis of human endothelial cells. Here, we demonstrate that the purified antibody is capable of inhibiting channel formation by human cancer cells, suggesting a common morphogenic pathway in both processes. Moreover, matrix-embedded cells producing antibody fragments may render the surrounding matrix non-permissive for aggressive tumor cells. These results open the way for the development of new therapeutic strategies for cancer.
Epidermolysis bullosa is a group of hereditary mechanobullous dermatoses in which detachment of the skin and mucosa in or around the epidermal basement membrane takes place from birth on. The clinical manifestations vary from abnormalities in the nails to painful mutilation of the skin, eyes, mouth, throat, oesophagus and locomotor apparatus. Ten genes have been identified that can cause a form of epidermolysis bullosa. These genes code for proteins in or around the hemidesmosome, the site of anchorage of the basal cell to the basement membrane. The prevalence of epidermolysis bullosa is about 1 in 22,000. The diagnosis is on the basis of the medical history, clinical findings, immunofluorescence microscopy, electron microscopy and DNA studies. The current treatment is still primarily symptomatic and prophylactic.
A 1-year-old boy with hemophagocytic lymphohistiocytosis exhibited proteinuria 1 month after unrelated cord blood cell transplantation, which persisted without hematuria. Laboratory study showed an increase of factor VIII-related antigen and total plasminogen activator inhibitor, suggesting endothelial injury. Histological examination of autopsy materials showed increased mesangial matrices and double-contoured basement membranes, and ultrastructurally, swelling of the endothelial cells and widening of the subendothelial space with mesangial interposition. Thrombosis was not observed at any of the sites. This case may be vasculopathy distinct from thrombotic microangiopathy (TMA) or a variant form of TMA following blood stem cell transplantation (BSCT). This vasculopathy should be considered in the differential diagnosis of proteinuria in the early stages after BSCT.