neurilemmoma/tyrosine

The aim of this study was to determine the relative utility of various preoperative diagnostic imaging modalities for the evaluation of benign schwannoma, including positron emission tomography (PET) utilising fluorine-18 fluoro-2-deoxy-D-glucose (FDG) and fluorine- 18 alpha-methyl tyrosine (FMT).

Background: High-grade glioma is the most pervasive and lethal of all brain malignancies. Despite advances in imaging technologies, discriminating between gliomas and other brain diseases such as multiple sclerosis (MS) often requires

Over-expression of the erbB2-receptor tyrosine kinase is frequently observed in many human tumors of epithelial origin. Due to its causal involvement in malignant transformation and its presence on the tumor cell surface erbB2 is an attractive target for directed tumor therapy. We earlier described

OBJECTIVE To investigate the early events in molecular progression toward schwannoma tumorigenesis, we developed an in vitro model of human Schwann cell tumorigenesis by merlin knockdown. BACKGROUND Neurofibromatosis 2 (NF2)-related and sporadic vestibular schwannoma (VS) exhibit loss of functional

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

Schwannomas that occur spontaneously or in patients with neurofibromatosis Type 2, lack both alleles for the tumor suppressor and plasma membrane-cytoskeleton linker merlin. We have shown that human primary schwannoma cells display activation of the RhoGTPases Rac1 and Cdc42 which results in highly

We studied the potential of PET with L-[1-11C]-tyrosine (TYR) to visualize tumors outside the central nervous system and to quantify their protein synthesis rates (PSRs). METHODS Twenty-two patients suspected of having a malignant tumor underwent a PET study with TYR before biopsy. The PSR in

The neurofibromatosis 2 tumor suppressor protein schwannomin/merlin is commonly mutated in schwannomas and meningiomas. Schwannomin, a member of the 4.1 family of proteins, which are known to link the cytoskeleton to the plasma membrane, has little known function other than its ability to suppress

The NF2 gene encodes the tumour suppressor protein merlin. The mutation of a single allele of this gene causes the autosomal dominantly inherited disease neurofibromatosis type 2 (NF2), which is characterized mainly by vestibular schwannoma carrying a second hit mutation. Complete lack of merlin is

Axons damaged in the adult mammalian central nervous system are able to regenerate when their inhibitory glial environment is replaced with a more permissive substrate. Here, we have used long oblique "bridge" grafts of fibroblast growth factor-4-transfected RN-22 schwannoma cells to allow

Hepatocyte growth factor-regulated tyrosine kinase substrate (HRS) is required for trafficking of cell surface receptors to the lysosome. Previously, we identified HRS as a protein that interacts with the neurofibromatosis 2 tumor suppressor schwannomin. In the present study, we established modified

Loss of the tumor suppressor protein merlin causes a variety of benign tumors such as schwannomas, meningiomas, and gliomas in man. We previously reported primary human schwannoma cells to show enhanced integrin-dependent adhesion and a hyperactivation of the small RhoGTPase Rac1. Here we show that

OBJECTIVE Provide an overview of the literature on vestibular schwannoma biology with special attention to tumor behavior and targeted therapy. BACKGROUND Vestibular schwannomas are benign tumors originating from the eighth cranial nerve and arise due to inactivation of the NF2 gene and its product

The neurofibromatosis 2 tumor suppressor protein, merlin or schwannomin, functions as a negative growth regulator; however, its mechanism of action is not known. In an effort to determine how merlin regulates cell growth, we analyzed a recently identified novel merlin interactor, hepatocyte growth