Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper presents the case of a 65 year-old woman suffering from recurrent oral aphthoid ulcers which rapidly evolved towards hyperplastic and ulcerated lesions over the entire floor of the mouth. The initial lesions were interpreted as non-specific aphthoid ulcers. Later, a tentative diagnosis of necrotising stomatitis with secondary reactive proliferating epithelial hyperplasia was made. The clinical symptoms and the immuno-phenotyping of lymphocytes circulating in the peripheral blood suggested the diagnosis of CD30-positive large cell anaplastic lymphoma. The biopsy showed only a pseudoepitheliomatous hyperplasia, reactive infiltrates and no lymphoma cells. The disease ran a fulminant course leading to death within 4 weeks due to acute gastro-intestinal bleeding. Autopsy revealed infiltrates of CD30+ large cell anaplastic lymphoma in a submandibular lymph node, in a thrombus stenosing the right subclavian vein, in the spleen, the anterior and posterior gastric wall as well as in the depth of the tumour on the floor of the mouth. The clinical and histopathological spectrum of CD30+ large cell anaplastic lymphoma is considerably variable. The particular feature of pseudoepitheliomatous hyperplasia has been reported especially in CD30+ anaplastic large cell lymphomas. An early correct diagnosis is rendered difficult in insufficient biopsy size, becauses this type of lymphoma often simulates other inflammatory or neoplastic skin diseases. Thus, with a necrotising and hyperplastic gingivostomatitis, the diagnosis of a CD30+ anaplastic large cell lymphoma should be considered.
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PMID:Metastasising malignant lymphoma mimicking necrotising and hyperplastic gingivostomatitis. 1052 40

Lentiviral vectors (LV) are widely used to successfully transduce cells for research and clinical applications. Lentiviral vectors pseudotyped with the vesicular stomatitis virus glycoprotein (VSV-G) can be produced to high titers and mediate high transduction efficiencies in vitro. For clinical applications the need for optimized transduction protocols and the limited activity of retronectin as LV enhancer, results in the application of a high multiplicity of infection (MOI) to achieve effective transduction efficiencies for a number of therapeutically relevant cells, e.g. CD34(+) hematopoietic stem cells, T- and B-cells. Our study describes an optimized LV infection protocol including a non-toxic poloxamer-based adjuvant combined with antibody-retargeted lentiviral particles, improving transduction efficiency at low MOI. Cell specificity of lentiviral vectors was increased by displaying different ratios of scFv-fused VSV-G glycoproteins on the viral envelope. The system was validated with difficult to transduce human CD30(+) lymphoma cells, and EGFR(+) tumor cells. Highly efficient transduction of lymphoma cells was achieved, >50% of cells were transduced when MOI 1 was used. The scFv displaying lentiviral particles gained relative specificity for transduction of target cells. Preferential gene delivery to CD30(+) or EGFR(+) cells was increased 4-fold in mixed cell cultures by presenting scFv antibody fragments binding to respective surface markers. A combination of spinoculation, poloxamer-based chemical adjuvant, and LV displaying scFv fragments increases transduction efficiencies of hard-to-transduce suspension lymphoma cells, and promises new chances for the future development of improved clinical protocols.
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PMID:Systematic improvement of lentivirus transduction protocols by antibody fragments fused to VSV-G as envelope glycoprotein. 2452 98

Classical Hodgkin lymphoma (cHL) is a hematopoietic malignancy with a characteristic cellular composition. The tumor mass is made up of infiltrated lymphocytes and other cells of hematologic origin but only very few neoplastic cells that are mainly identified by the diagnostic marker CD30. While most patients with early stage cHL can be cured by standard therapy, treatment options for relapsed or refractory cHL are still not sufficient, although immunotherapy-based approaches for the treatment of cHL patients have gained ground in the last decade. Here, we suggest a novel therapeutic concept based on oncolytic viruses selectively destroying the CD30+-positive cHL tumor cells. Relying on a recently described CD30-specific scFv we have generated CD30-targeted measles virus (MV-CD30) and vesicular stomatitis virus (VSV-CD30). For VSV-CD30 the VSV glycoprotein G reading frame was replaced by those of the CD30-targeted MV glycoproteins. Both viruses were found to be highly selective for CD30-positive cells as demonstrated by infection of co-cultures of target and non-target cells as well as through blocking infection by soluble CD30. Notably, VSV-CD30 yielded much higher titers than MV-CD30 and resulted in a more rapid and efficient killing of cultivated cHL-derived cell lines. Mouse tumor models revealed that intratumorally, as well as systemically injected VSV-CD30, infected cHL xenografts and significantly slowed down tumor growth resulting in a substantially prolonged survival of tumor-bearing mice. Taken together, the data support further preclinical testing of VSV-CD30 as novel therapeutic agent for the treatment of cHL and other CD30+-positive malignancies.
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PMID:CD30-targeted oncolytic viruses as novel therapeutic approach against classical Hodgkin lymphoma. 2956 Jan 24