RESUMO
Malignant epithelioid hemangioendothelioma (MEH), also known as high-risk epithelioid hemangioendothelioma, is a low- to intermediate-grade vascular malignancy originally described as a vascular neoplasm of endothelial origin. This very rare vascular neoplasm has been described mainly in soft tissue, but also in various organs and locations, including the liver, lung, brain, colon, lymph nodes, peritoneum, spleen, bone, skin, heart, soft tissues, and vascular system. Several cases have been described in the head and neck, including the submandibular gland, parotid gland, nasal cavity, parapharyngeal space, maxilla, maxillary sinus, occipital bone, oral cavity, thyroid gland, neck, scalp, larynx, and mandible. This case report is the first description of MEH presenting as an exophytic lower-lip lesion.
Assuntos
Hemangioendotelioma Epitelioide/diagnóstico , Neoplasias Labiais/diagnóstico , Biópsia , Núcleo Celular/ultraestrutura , Citoplasma/ultraestrutura , Diagnóstico Diferencial , Epitélio/patologia , Feminino , Seguimentos , Humanos , Lábio/cirurgia , Pessoa de Meia-Idade , Gradação de Tumores , Úlceras Orais/diagnósticoRESUMO
We report in this study on the isolation and expansion of neural crest stem cells (NCSCs) from the epithelium of oral mucosa (OM) using reagents that are GMP-certified and FDA-approved for clinical use. Characterization analysis showed that the levels of keratins K2, K6C, K4, K13, K31, and K15-specific to OM epithelial cells-were significantly lower in the experimental NCSCs. While SOX10 was decreased with no statistically significant difference, the earliest neural crest specifier genes SNAI1/2, Ap2a, Ap2c, SOX9, SOX30, Pax3, and Twist1 showed a trend in increased expression in NCSCs. In addition, proteins of Oct4, Nestin and Noth1 were found to be greatly expressed, confirming NCSC multipotency. In conclusion, our study showed that the epithelium of OM contains NCSCs that can be isolated and expanded with clinical-grade reagents to supply the demand for multipotent cells required for clinical applications in regenerative medicine. Supported by Emmaus Medical Inc.
Assuntos
Crista Neural , Células-Tronco Neurais , Humanos , Crista Neural/metabolismo , Mucosa Bucal , Células-Tronco Neurais/metabolismo , Células-Tronco Multipotentes/metabolismo , Proteínas Supressoras de Tumor/metabolismo , Fatores de Transcrição SOX/metabolismoRESUMO
Cyclophilin A (CypA) was originally identified as a cytosolic protein possessing peptidyl-prolyl isomerase activity. CypA has been shown to play a pivotal role in the immune response, but little is known about other molecular mechanisms of CypA-mediated biologic events. In our present study, we demonstrate that knockdown CypA expression using RNAi in U2OS cells resulted in disruption of the F-actin structure, as well as decreased anchorage-independent growth, proliferation, and migration. Wild-type U2OS cells treated with cyclosporine A (CsA), a peptidyl-prolyl isomerase inhibitor, displayed the same phenotype as knockdown CypA cells, suggesting that the isomerase activity of CypA is required to maintain a normal phenotype. In vitro and in vivo binding assays revealed that CypA binds to N-WASP, which functions in the nucleation of actin via the Arp2/3 complex. Pulse-chase labeling study indicated an enhanced degradation of N-WASP in cell lacking CypA, suggesting that CypA is required for stabilizing N-WASP to form a N-WASP/Arp2/3 complex for the nucleation/initiation of F-actin polymerization.
Assuntos
Actinas/química , Ciclofilina A , Técnicas de Silenciamento de Genes , Neoplasias , RNA Interferente Pequeno , Actinas/metabolismo , Animais , Linhagem Celular Tumoral , Movimento Celular/fisiologia , Ciclofilina A/genética , Ciclofilina A/metabolismo , Inativação Gênica , Humanos , Neoplasias/metabolismo , Neoplasias/patologia , RNA Interferente Pequeno/genética , RNA Interferente Pequeno/metabolismo , Proteína Neuronal da Síndrome de Wiskott-Aldrich/genética , Proteína Neuronal da Síndrome de Wiskott-Aldrich/metabolismoAssuntos
Indutores da Angiogênese/uso terapêutico , Mandíbula/cirurgia , Fator de Crescimento Derivado de Plaquetas/uso terapêutico , Retalhos Cirúrgicos/patologia , Deiscência da Ferida Operatória/tratamento farmacológico , Cicatrização/efeitos dos fármacos , Adolescente , Aumento do Rebordo Alveolar , Becaplermina , Transplante Ósseo/patologia , Rotulagem de Medicamentos , Sobrevivência de Enxerto/efeitos dos fármacos , Sobrevivência de Enxerto/fisiologia , Humanos , Masculino , Mandíbula/patologia , Procedimentos Cirúrgicos Pré-Protéticos Bucais/métodos , Proteínas Proto-Oncogênicas c-sis , Proteínas Recombinantes , Retalhos Cirúrgicos/irrigação sanguínea , Resultado do Tratamento , Cicatrização/fisiologia , Adulto JovemRESUMO
Nitrogen-containing and non-nitrogen-containing bisphosphonates have been implicated in the development of osteonecrosis of the jaw (ONJ), a condition termed bisphosphonate-related OHJ. Other antiresorptive drugs have been implicated in the development of OHJ, hence the new term antiresorptive drug-related ONJ. The underlying pathogenesis remains unclear, and no definite diagnosis or cure has been established for this debilitating condition. This article reviews some of the most common antiresorptive drugs with their associated risks of ONJ and the current understanding of the pathogenesis ONJ, and summarizes current clinical guidelines.