neurofibroma/tyrosine

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Imatinib mesylate (Glivec) inhibits Schwann cell viability and reduces the size of human plexiform neurofibroma in a xenograft model.

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Plexiform neurofibromas (PNF), one of the major features of neurofibromatosis type 1 (NF1), are characterized by complex cellular composition and mostly slow but variable growth patterns. In this study, we examined the effect of imatinib mesylate, a receptor tyrosine kinase inhibitor, on PNF-derived

Pediatric PK/PD Phase I Trial of Pexidartinib in Relapsed and Refractory Leukemias and Solid Tumors Including Neurofibromatosis Type I related Plexiform Neurofibromas

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Purpose: Simultaneously targeting the tumor and tumor microenvironment (TME) may hold promise in treating children with refractory solid tumors. Pexidartinib, an oral inhibitor of tyrosine kinases including Colony Stimulating Factor 1

Nilotinib is more potent than imatinib for treating plexiform neurofibroma in vitro and in vivo.

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Plexiform neurofibromas (PNFs) are benign nerve sheath tumors mostly associated with neurofibromatosis type 1. They often extend through multiple layers of tissue and therefore cannot be treated satisfactorily by surgery. Nilotinib is a tyrosine kinase inhibitor used to treat leukemia, with

Neurotransmitter analysis of dermal neurofibromas: implications for the pathogenesis and treatment of neurofibromatosis.

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We examined 15 dermal neurofibromas from five adults with disseminated neurofibromatosis. All tumors contained axons that reacted for catecholamines and tyrosine hydroxylase on histochemical stains. Assay of tissue homogenates identified norepinephrine as the catecholamine. Assays for dopamine and

Pigmented neurofibroma: review of Japanese patients with an analysis of melanogenesis demonstrating coexpression of c-met protooncogene and microphthalmia-associated transcription factor.

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Pigmented neurofibroma (PNF) is a rare variant of neurofibroma showing melanin production. To clarify the clinicopathologic features of PNF and to characterize melanogenesis in PNF, 12 cases of PNF were examined in comparison with schwannoma (SCH, n = 16) and neurofibroma (NF, n = 26). The PNF

Nf1 mutation expands an EGFR-dependent peripheral nerve progenitor that confers neurofibroma tumorigenic potential.

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Defining growth factor requirements for progenitors facilitates their characterization and amplification. We characterize a peripheral nervous system embryonic dorsal root ganglion progenitor population using in vitro clonal sphere-formation assays. Cells differentiate into glial cells, smooth

Targetable ERBB2 mutations identified in neurofibroma/schwannoma hybrid nerve sheath tumors.

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Neurofibroma/schwannoma hybrid nerve sheath tumors (N/S HNSTs) are neoplasms associated with larger nerves that occur sporadically and in the context of schwannomatosis or neurofibromatosis type 2 or 1. Clinical management of N/S HNST is challenging, especially for large tumors, and

EGFR-Stat3 signalling in nerve glial cells modifies neurofibroma initiation.

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Neurofibromatosis type 1 (NF1) is an inherited disease in which affected patients are predisposed to develop benign Schwann cell (SC) tumours called neurofibromas. In the mouse, loss of Nf1 in the SC lineage causes neurofibroma formation. The tyrosine kinase receptor EGFR is expressed in Schwann

Paraspinal neurofibromas and hypertrophic neuropathy in Noonan syndrome with multiple lentigines.

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BACKGROUND Noonan syndrome with multiple lentigines (NSML), formerly known as LEOPARD syndrome, is an autosomal-dominant disorder characterised by lentigines, EKG abnormalities, ocular hypertelorism, pulmonic stenosis, abnormal genitalia, growth retardation and deafness. There is significant

Imatinib mesylate inhibits cell invasion of malignant peripheral nerve sheath tumor induced by platelet-derived growth factor-BB.

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Malignant peripheral nerve sheath tumor (MPNST) is rare, highly aggressive, resistant to radiochemotherapy, and associated with poor prognosis. Basic research to develop new treatment regimes is critically needed. This study was designed to identify motogenic factor(s) involved in MPNST cell

Neurofibromatosis type 1 and GIST: is there a correlation?

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BACKGROUND Neurofibromatosis type 1 (NF1) is a hereditary cancer predisposition syndrome characterized by neurologic, dermatologic and orthopedic manifestations. There is a spectrum of tumors that affects individuals with NF1 at an increased incidence compared to the general population, such as

Expression of Kit in neurofibromin-deficient human Schwann cells: role in Schwann cell hyperplasia associated with type 1 neurofibromatosis.

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Type 1 Neurofibromatosis (NF1) is characterized by the formation of neurofibromas, benign tumors composed mainly of Schwann cells, which can turn malignant to form neurofibrosarcomas. Neurofibromin, the protein product of the Nf1 gene, is believed to act as a tumor suppressor, accelerating the

Epidermal growth factor receptor is not amplified in schwannomas.

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Epidermal growth factor receptor (EGFR) is a tyrosine kinase receptor of the ErbB family. This family of receptors plays an active role in cellular growth and mitogenesis. It is well established that the overexpression of ErbB receptors in human cancers, most commonly because of true genomic

[Development of thymic tumor in HTLV-I transgenic rats under control of a lymphoid tissue specific promoter].

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The p40tax protein of Human T lymphocyte virus type I (HTLV-I) is known to be a transactivator not only for the own viral gene but also for the various cellular genes (host genes), including a number of cytokine genes and genes for cell proliferation. Its tumorigenicity was also reported in vivo,

Neoplasms of the peripheral nervous system.

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Neoplasms of the peripheral nervous system arise from the cellular sheath surrounding the nerve trunks, that is, the pluripotential Schwann cells and related cells, and rarely affect the feet. When present, they are most frequently associated with the autosomal dominantly inherited neurofibromatosis

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