11 research outputs found
Microsporum canis infection mimics pemphigus erythematosus
We report a 55-year-old Japanese woman with a two-month history of multiple pruritic erythema and erosion on her face and neck. Based on the clinical appearance, we initially diagnosed her as having pemphigus erythematosus. However, the results of a histopathological examination and a direct immunofluorescence study did not support the initial diagnosis. Additionally, anti-desmoglein 1 and 3 antibodies were all negative. Subsequently, a microscopic examination of scales revealed filaments of fungi and a fungal culture was negative for macroconidium. Using molecular biology techniques, we identified the fungus as Microsporum canis, which causes a zoonotic infection. The immune reaction to the fungi could be drastic and therefore, the eruption sometimes displays atypical clinical manifestations
Recurrent advanced rectal malignant melanoma that discontinued anti‐PD‐1 antibody after complete response and was refractory to rechallenge
Tranilast inhibits the expression of genes related to epithelial-mesenchymal transition and angiogenesis in neurofibromin-deficient cells
Abstract Neurofibromatosis type 1 (NF1) is caused by germline mutations in the NF1 gene and is characterized by café au lait spots and benign tumours known as neurofibromas. NF1 encodes the tumour suppressor protein neurofibromin, which negatively regulates the small GTPase Ras, with the constitutive activation of Ras signalling resulting from NF1 mutations being thought to underlie neurofibroma development. We previously showed that knockdown of neurofibromin triggers epithelial-mesenchymal transition (EMT) signalling and that such signalling is activated in NF1-associated neurofibromas. With the use of a cell-based drug screening assay, we have now identified the antiallergy drug tranilast (N-(3,4-dimethoxycinnamoyl) anthranilic acid) as an inhibitor of EMT and found that it attenuated the expression of mesenchymal markers and angiogenesis-related genes in NF1-mutated sNF96.2 cells and in neurofibroma cells from NF1 patients. Tranilast also suppressed the proliferation of neurofibromin-deficient cells in vitro more effectively than it did that of intact cells. In addition, tranilast inhibited sNF96.2 cell migration and proliferation in vivo. Knockdown of type III collagen (COL3A1) also suppressed the proliferation of neurofibroma cells, whereas expression of COL3A1 and SOX2 was increased in tranilast-resistant cells, suggesting that COL3A1 and the transcription factor SOX2 might contribute to the development of tranilast resistance