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1
acoustic neurofibromatoses bilateral 2005:2010[pubdate] *count=100
607 results
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Items 1 to 100 of about 607
1.
Evans DG, Watson C, King A, Wallace AJ, Baser ME:
Multiple meningiomas: differential involvement of the NF2 gene in children and adults.
J Med Genet
; 2005 Jan;42(1):45-8
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[Title]
Multiple meningiomas: differential involvement of the
NF2
gene in children and adults.
OBJECTIVE: To screen for
NF2
mutations in people with meningiomas.
METHODS: Lymphocyte or tumour DNA was analysed from 46 individuals from 36 families who presented with a meningioma at age < or =15 years without
vestibular schwannoma
(VS), or who had multiple meningiomas in adulthood before the
diagnosis
of vs.
RESULTS: Eight of 13 people with meningioma and other features of
neurofibromatosis 2
(
NF2
) had an identified constitutional
NF2
mutation in blood DNA, but none of the other subjects had identified constitutional
NF2
mutations.
CONCLUSIONS: Constitutional
NF2
mutations are the most likely cause of meningioma in children and in people with a meningioma plus other non-VS features of
NF2
.
Mosaic
NF2
may be the cause of about 8% of multiple meningiomas in sporadic adult cases, but there are other causes in the majority of other such patients and in multiple meningioma in families.
[MeSH-major]
Genes,
Neurofibromatosis 2
. Meningioma / genetics. Mutation.
Neuroma
,
Acoustic
/ genetics. Point Mutation
[MeSH-minor]
Adolescent. Adult. Child. Humans. Loss of Heterozygosity. Mosaicism.
Neurofibromatosis 2
/ genetics. Polymerase Chain Reaction
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[Cites]
J Pathol. 2001 Jul;194(3):367-72
[
11439370.001
]
[Cites]
J Neurosurg. 2001 Jan;94(1):111-7
[
11147878.001
]
[Cites]
J Neuropathol Exp Neurol. 2000 Oct;59(10):872-9
[
11079777.001
]
[Cites]
Hum Mol Genet. 2000 Jun 12;9(10):1495-500
[
10888600.001
]
[Cites]
J Neuropathol Exp Neurol. 2000 Jun;59(6):504-12
[
10850863.001
]
[Cites]
J Neurosurg. 2000 May;92(5):766-70
[
10794289.001
]
[Cites]
Neurology. 2000 Jan 11;54(1):71-6
[
10636128.001
]
[Cites]
Arch Dis Child. 1999 Dec;81(6):496-9
[
10569966.001
]
[Cites]
J Neuropathol Exp Neurol. 2001 Oct;60(10):994-1003
[
11589430.001
]
[Cites]
Genet Test. 1999;3(2):173-83
[
10464665.001
]
[Cites]
Neurosurgery. 1999 Aug;45(2):409-16
[
10449091.001
]
[Cites]
Oncogene. 1999 Apr 1;18(13):2231-9
[
10327069.001
]
[Cites]
Am J Hum Genet. 1998 Sep;63(3):727-36
[
9718334.001
]
[Cites]
Cancer Res. 1998 Aug 1;58(15):3226-30
[
9699646.001
]
[Cites]
J Neurosurg. 1998 Mar;88(3):562-9
[
9488313.001
]
[Cites]
J Neurooncol. 1996 Sep;29(3):197-205
[
8858525.001
]
[Cites]
J Neurosurg. 1996 May;84(5):847-51
[
8622160.001
]
[Cites]
Neurology. 1993 Oct;43(10):2096-8
[
8413972.001
]
[Cites]
Q J Med. 1992 Aug;84(304):603-18
[
1484939.001
]
[Cites]
Hum Pathol. 2002 Mar;33(3):375-8
[
11979381.001
]
[Cites]
J Neurosurg. 2002 Nov;97(5):1078-82
[
12450029.001
]
[Cites]
Int J Cancer. 2003 Feb 10;103(4):483-8
[
12478663.001
]
[Cites]
J Med Genet. 2003 Jun;40(6):459-63
[
12807969.001
]
[Cites]
J Med Genet. 1992 Dec;29(12):841-6
[
1479598.001
]
(PMID = 15635074.001).
[ISSN]
1468-6244
[Journal-full-title]
Journal of medical genetics
[ISO-abbreviation]
J. Med. Genet.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC1735900
2.
Kokkinakis DM, Liu X, Neuner RD:
Modulation of cell cycle and gene expression in pancreatic tumor cell lines by methionine deprivation (methionine stress): implications to the therapy of pancreatic adenocarcinoma.
Mol Cancer Ther
; 2005 Sep;4(9):1338-48
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Although methionine stress-induced toxicity is not solely dependent on p53, the gain in p21 and loss in CDK1 transcription are more enhanced in wild-
type
p53 tumors.
Cell cycle and mitotic arrest is in agreement with up-regulation of
NF2
, ETS2, CLU, GADD45alpha, GADD45beta, and GADD45gamma and down-regulation of AURKB, TOP2A, CCNA, CCNB, PRC1, BUB1, NuSAP, IFI16, and BRCA1.
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Hazardous Substances Data Bank.
DACARBAZINE
.
Hazardous Substances Data Bank.
FLUOROURACIL
.
Hazardous Substances Data Bank.
(L)-Methionine
.
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(PMID = 16170025.001).
[ISSN]
1535-7163
[Journal-full-title]
Molecular cancer therapeutics
[ISO-abbreviation]
Mol. Cancer Ther.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Neoplasm Proteins; 0 / Retinoblastoma Protein; 0 / Transforming Growth Factor beta; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; AE28F7PNPL / Methionine; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; U3P01618RT / Fluorouracil
3.
Combs SE, Thilmann C, Debus J, Schulz-Ertner D:
Long-term outcome of stereotactic radiosurgery (SRS) in patients with acoustic neuromas.
Int J Radiat Oncol Biol Phys
; 2006 Apr 1;64(5):1341-7
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[Title]
Long-term outcome of stereotactic radiosurgery (SRS) in patients with
acoustic
neuromas.
PURPOSE: To evaluate the effectiveness and long-term outcome of stereotactic radiosurgery (SRS) for
acoustic
neuromas (AN).
Two patients suffered from
neurofibromatosis type
2.
[MeSH-major]
Hearing / radiation effects.
Neuroma
,
Acoustic
/ surgery. Radiosurgery
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Facial Nerve / radiation effects. Facial Paralysis / etiology. Female. Hearing Loss / etiology. Humans. Male. Middle Aged.
Neurofibromatosis 2
/ complications. Radiation Injuries / etiology. Trigeminal Neuralgia / etiology
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.
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(PMID = 16464537.001).
[ISSN]
0360-3016
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
United States
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4.
Roche PH, Bouvier C, Chinot O, Figarella-Branger D:
Genesis and biology of vestibular schwannomas.
Prog Neurol Surg
; 2008;21:24-31
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[Title]
Genesis and biology of
vestibular
schwannomas.
This review chapter is a synthesis of the recent literature about pathogenesis of schwannomas with emphasis on
vestibular
schwannomas (VSs).
The understanding of this mechanism has been gained from molecular genetic studies of
neurofibromatosis type
2 (
NF2
) patients, in whom mutations of a tumor suppressor gene (
NF2
gene) was clearly identified.
S/M is the normal
NF2
gene product.
Lack of normal S/M protein in the
schwannoma
cell is due to gene mutation in 50% of sporadic VSs.
Apart from the involvement of the S/M pathway, the authors review the potential role of other genetic abnormalities and growing factors that are supposed to be involved in the pathogenesis of vs. Understanding the pathways of action and regulation of S/M may provide the basics for identifying potential therapeutic targets, which is of paramount importance for a better management of
NF2
patients.
[MeSH-major]
Genes,
Neurofibromatosis 2
/ physiology. Neurofibromin 2 / physiology.
Neuroma
,
Acoustic
/ genetics.
Neuroma
,
Acoustic
/ pathology
[MeSH-minor]
Epigenesis, Genetic / physiology. Humans.
Neurofibromatosis 2
/ complications.
Neurofibromatosis 2
/ genetics
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(PMID = 18810196.001).
[ISSN]
0079-6492
[Journal-full-title]
Progress in neurological surgery
[ISO-abbreviation]
Prog Neurol Surg
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Neurofibromin 2
[Number-of-references]
43
5.
Cunningham CD 3rd, Friedman RA, Brackmann DE, Hitselberger WE, Lin HW:
Neurotologic skull base surgery in pediatric patients.
Otol Neurotol
; 2005 Mar;26(2):231-6
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OBJECTIVE: Innovations in
diagnosis
, surgical techniques, and perioperative care have dramatically improved outcomes in
lateral
skull base procedures in recent years.
PATIENTS: Eighty-nine pediatric patients undergoing 115 neurotologic procedures for
lateral
skull base tumors from July 1992 to September 2003.
MAIN OUTCOME MEASURES: Initial clinical presentation, tumor
type
, pre- and postoperative hearing and facial nerve status, treatment course, complications, and functional outcomes.
RESULTS: The majority of tumors in this series were
vestibular
schwannomas, and 65 patients were diagnosed with
neurofibromatosis Type
2.
Complete tumor removal was accomplished in the majority of cases (97%), with good preservation of facial nerve function (House-Brackmann Grade I or
II
) in 80% of patients.
CONCLUSION: With advances in diagnostic procedures and use of current neurotologic techniques, pediatric patients may undergo successful treatment of
lateral
skull base tumors, with good functional outcomes and minimal morbidity.
[MeSH-major]
Neurofibromatosis 2
/ surgery.
Neuroma
,
Acoustic
/ surgery. Postoperative Complications / etiology. Skull Base / surgery. Skull Base Neoplasms / surgery
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(PMID = 15793410.001).
[ISSN]
1531-7129
[Journal-full-title]
Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology
[ISO-abbreviation]
Otol. Neurotol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
6.
Hasegawa T, Fujitani S, Katsumata S, Kida Y, Yoshimoto M, Koike J:
Stereotactic radiosurgery for vestibular schwannomas: analysis of 317 patients followed more than 5 years.
Neurosurgery
; 2005 Aug;57(2):257-65; discussion 257-65
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[Title]
Stereotactic radiosurgery for
vestibular
schwannomas: analysis of 317 patients followed more than 5 years.
OBJECTIVE: Many investigators have reported successful treatment of
vestibular
schwannomas with gamma knife radiosurgery (GKRS).
However, long-term outcomes should be evaluated before concluding that GKRS is truly safe and effective for the treatment of
vestibular
schwannomas.
METHODS: Between May 1991 and December 1998, 346 consecutive patients (excluding those presenting with
neurofibromatosis Type
2) were treated with GKRS.
[MeSH-major]
Cranial Nerve Neoplasms / surgery.
Neuroma
,
Acoustic
/ surgery. Radiosurgery / methods. Treatment Outcome
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(PMID = 16094154.001).
[ISSN]
1524-4040
[Journal-full-title]
Neurosurgery
[ISO-abbreviation]
Neurosurgery
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article
[Publication-country]
United States
7.
Sharma MS, Singh R, Kale SS, Agrawal D, Sharma BS, Mahapatra AK:
Tumor control and hearing preservation after Gamma Knife radiosurgery for vestibular schwannomas in neurofibromatosis type 2.
J Neurooncol
; 2010 Jun;98(2):265-70
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[Title]
Tumor control and hearing preservation after Gamma Knife radiosurgery for
vestibular
schwannomas in
neurofibromatosis type
2.
To analyze the effect of Gamma Knife radiosurgery (GKS) on tumor control and hearing preservation rates in patients with
vestibular
schwannomas (VS) in a setting of
neurofibromatosis type
2 (
NF 2
), a retrospective study was carried out at a tertiary-level referral Gamma Knife unit.
Dose plans, pre- and postoperative radiology, and follow-up clinical records of patients with
NF 2
who had undergone GKS for VS using a Leksell Gamma Knife (Elekta Instruments AB, Stockholm, Sweden) model B unit from 1997 to 2008 were reviewed.
Twenty-four patients had
bilateral
vs. The commonest clinical presentation was hearing loss and tinnitus.
GKS for VS provides satisfactory tumor control and hearing preservation in patients with
NF 2
.
[MeSH-major]
Hearing / physiology.
Neurofibromatosis 2
/ surgery. Radiosurgery / methods
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[ISSN]
1573-7373
[Journal-full-title]
Journal of neuro-oncology
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J. Neurooncol.
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eng
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Journal Article
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United States
8.
Niv MY, Iida K, Zheng R, Horiguchi A, Shen R, Nanus DM:
Rational redesign of neutral endopeptidase binding to merlin and moesin proteins.
Protein Sci
; 2009 May;18(5):1042-50
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Here we show that the ERM-related protein merlin (
NF2
) does not bind NEP or its cytosolic region.
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[ISSN]
1469-896X
[Journal-full-title]
Protein science : a publication of the Protein Society
[ISO-abbreviation]
Protein Sci.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA80240; United States / NCI NIH HHS / PC / PC040758
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Microfilament Proteins; 0 / Neurofibromin 2; 0 / Peptides; 144131-77-1 / moesin; EC 3.4.24.11 / Neprilysin
[Other-IDs]
NLM/ PMC2771306
9.
Thomas R, Duke SE, Wang HJ, Breen TE, Higgins RJ, Linder KE, Ellis P, Langford CF, Dickinson PJ, Olby NJ, Breen M:
'Putting our heads together': insights into genomic conservation between human and canine intracranial tumors.
J Neurooncol
; 2009 Sep;94(3):333-49
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Interestingly, however, genomic imbalances orthologous to some of the hallmark aberrations of human intracranial tumors, including chromosome 22/
NF2
deletions in meningiomas and chromosome 1p/19q deletions in oligodendrogliomas, were not major events in the dog.
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[ISSN]
1573-7373
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
ENG
[Grant]
United States / NINDS NIH HHS / NS / NS051190-01; United States / NINDS NIH HHS / NS / R21 NS051190; United States / NINDS NIH HHS / NS / R21 NS051190-01; United States / NINDS NIH HHS / NS / NS051190; United Kingdom / Wellcome Trust / /
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ NIHMS183408; NLM/ PMC3225023
10.
McLaughlin ME, Kruger GM, Slocum KL, Crowley D, Michaud NA, Huang J, Magendantz M, Jacks T:
The Nf2 tumor suppressor regulates cell-cell adhesion during tissue fusion.
Proc Natl Acad Sci U S A
; 2007 Feb 27;104(9):3261-6
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[Title]
The
Nf2
tumor suppressor regulates cell-cell adhesion during tissue fusion.
We found that in the mouse embryo, expression of the
Nf2
tumor suppressor, merlin, is dynamically regulated during tissue fusion:
Nf2
expression is low at the leading front before fusion and high across the fused tissue bridge.
Mosaic
Nf2
mutants exhibit a global defect in tissue fusion characterized by ectopic detachment and increased detachment-induced apoptosis (anoikis).
Our work reveals that regulation of
Nf2
expression is a previously unrecognized means of controlling adhesion at the leading front, thereby ensuring successful tissue fusion.
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[
10753521.001
]
(PMID = 17360635.001).
[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; 0 / Neurofibromin 2
[Other-IDs]
NLM/ PMC1801999
11.
Barski D, Wolter M, Reifenberger G, Riemenschneider MJ:
Hypermethylation and transcriptional downregulation of the TIMP3 gene is associated with allelic loss on 22q12.3 and malignancy in meningiomas.
Brain Pathol
; 2010 May;20(3):623-31
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We performed direct sodium bisulfite sequencing in a series of 50 meningiomas, including 27 benign meningiomas [World Health Organization (WHO) grade I], 11 atypical meningiomas (WHO grade
II
) and 12 anaplastic meningiomas (WHO grade III), and found hypermethylation of TIMP3 in 67% of anaplastic meningiomas, but only 22% of atypical and 17% of benign meningiomas.
TIMP3 is located in the chromosomal band 22q12, the allelic loss of which occurs early in meningioma tumorigenesis and preferentially targets the
NF2
tumor suppressor gene.
Thus, TIMP3 inactivation by methylation seems fairly exclusive to meningiomas with allelic losses on 22q12 but--in contrast to
NF2
mutation--appears to be involved in meningioma progression as it is associated with a more aggressive, high-grade meningioma phenotype.
[MeSH-minor]
Aged. Aged, 80 and over. Cell Line, Tumor.
Disease
Progression. Down-Regulation / genetics. Humans. Male. Middle Aged
The Lens.
Cited by Patents in
.
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(PMID = 19922547.001).
[ISSN]
1750-3639
[Journal-full-title]
Brain pathology (Zurich, Switzerland)
[ISO-abbreviation]
Brain Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / TIMP3 protein, human; 0 / Tissue Inhibitor of Metalloproteinase-3
12.
Shen Y, Nunes F, Stemmer-Rachamimov A, James M, Mohapatra G, Plotkin S, Betensky RA, Engler DA, Roy J, Ramesh V, Gusella JF:
Genomic profiling distinguishes familial multiple and sporadic multiple meningiomas.
BMC Med Genomics
; 2009 Jul 09;2:42
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[Title]
Genomic profiling distinguishes
familial
multiple and sporadic multiple meningiomas.
BACKGROUND: Meningiomas may occur either as
familial
tumors in two distinct disorders,
familial
multiple meningioma and
neurofibromatosis 2
(
NF2
), or sporadically, as either single or multiple tumors in individuals with no family history.
Meningiomas in
NF2
and approximately 60% of sporadic meningiomas involve inactivation of the
NF2
locus, encoding the tumor suppressor merlin on chromosome 22q.
This study was undertaken to establish whether genomic profiling could distinguish
familial
multiple meningiomas from sporadic solitary and sporadic multiple meningiomas.
METHODS: We compared 73 meningiomas presenting as sporadic solitary (64), sporadic multiple (5) and
familial
multiple (4) tumors using genomic profiling by array comparative genomic hybridization (array CGH).
RESULTS: Sporadic solitary meningiomas revealed genomic rearrangements consistent with at least two mechanisms of tumor initiation, as unsupervised cluster analysis readily distinguished tumors with chromosome 22 deletion (associated with loss of the
NF2
tumor suppressor) from those without chromosome 22 deletion.
Whereas sporadic meningiomas without chromosome 22 loss exhibited fewer chromosomal imbalance events overall, tumors with chromosome 22 deletion further clustered into two major groups that largely, though not perfectly, matched with their benign (WHO Grade I) or advanced (WHO Grades
II
and III) histological grade, with the latter exhibiting a significantly greater degree of genomic imbalance (P < 0.001).
By contrast,
familial
multiple meningiomas displayed no imbalances, supporting a distinct mechanism for the origin for these tumors.
Most importantly, the striking difference observed between sporadic and
familial
multiple meningiomas indicates that genomic profiling can provide valuable information for differential
diagnosis
of subjects with multiple meningiomas and for considering the risk for tumor occurrence in their family members.
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(PMID = 19589153.001).
[ISSN]
1755-8794
[Journal-full-title]
BMC medical genomics
[ISO-abbreviation]
BMC Med Genomics
[Language]
ENG
[Grant]
United States / NINDS NIH HHS / NS / P01 NS024279
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2716362
13.
Nascimento AF, Fletcher CD:
The controversial nosology of benign nerve sheath tumors: neurofilament protein staining demonstrates intratumoral axons in many sporadic schwannomas.
Am J Surg Pathol
; 2007 Sep;31(9):1363-70
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This concept has recently been disputed in cases associated with
neurofibromatosis type
2.
The amount (rare, focal, multifocal, and diffuse) and distribution (
central
and/or peripheral) of axons within the tumors were analyzed.
NFP-positive axons were identified in 11 of 20 (55%) conventional schwannomas (2 rare, 4 focal, 3 multifocal, and 2 diffuse; 5
central
, 4 peripheral, and
2 central
and peripheral) and in 15 of 20 (75%) cellular schwannomas (3 rare, 6 focal, and 6 multifocal; 12
central
, 1 peripheral, and
2 central
and peripheral).
Of the 20 ancient schwannomas, 7 cases (35%) showed intratumoral axons, highlighted by NFP immunostaining (1 rare, 4 focal, 1 multifocal, and 1 diffuse; 4 peripheral,
2 central
, and 1
central
and peripheral).
Most cases of gastric
schwannoma
showed no evidence of intratumoral axons; 9 cases (90%) were negative for NFP and only 1 case (10%) was positive (focal and
central
).
Seven of 10 cases (70%) of plexiform schwannomas were negative for NFP, whereas only 3 cases (30%) showed positive axons (2 multifocal and 1 focal; 3
central
).
Although NFP-positive axons were most often present in the conventional and cellular variants of
schwannoma
, their presence was also observed in a minority of ancient, gastric and plexiform schwannomas.
Differentiation between neurofibroma and
schwannoma
in cases with overlapping cytoarchitectural features should not be based solely on the presence or absence of NFP-positive axons within a given tumor.
[MeSH-major]
Axons / chemistry. Neurilemmoma /
diagnosis
. Neurofibroma /
diagnosis
. Neurofilament Proteins / analysis. S100 Proteins / analysis. Schwann Cells / chemistry. Stomach Neoplasms /
diagnosis
[MeSH-minor]
Cell Differentiation. Cell Proliferation.
Diagnosis
, Differential. Humans. Immunohistochemistry. Neoplasm Invasiveness. Predictive Value of Tests. Reproducibility of Results
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(PMID = 17721192.001).
[ISSN]
0147-5185
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Neurofilament Proteins; 0 / S100 Proteins
14.
Lenarz T, Lim HH, Reuter G, Patrick JF, Lenarz M:
The auditory midbrain implant: a new auditory prosthesis for neural deafness-concept and device description.
Otol Neurotol
; 2006 Sep;27(6):838-43
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The auditory midbrain implant (AMI) is a new
central
auditory prosthesis designed for penetrating stimulation of the human inferior colliculus.
The major group of candidates for the AMI consists of
neurofibromatosis type
2 (
NF2
) patients who develop neural deafness because of growth and/or surgical removal of
bilateral acoustic
neuromas.
However, speech perception performance in
NF2
ABI patients has been limited.
The fact that the ABI is able to produce high levels of speech perception in nontumor patients (with inaccessible cochleae or posttraumatic damage to the cochlear nerve) suggests that limitations in ABI performance in
NF2
patients may be associated with cochlear nucleus damage caused by the tumors or the tumor removal process.
Thus, stimulation of the auditory midbrain proximal to the damaged cochlear nucleus may be a better alternative for hearing restoration in
NF2
patients.
We propose the
central
nucleus of the inferior colliculus (ICC) as the potential site.
The goal of this article is to present the ICC as an alternative site for an auditory implant for
NF2
patients and to describe the design of the first human prototype AMI.
[MeSH-minor]
Algorithms. Auditory Brain Stem Implants. Humans.
Neurofibromatosis 2
/ complications.
Neuroma
,
Acoustic
/ complications.
Neuroma
,
Acoustic
/ etiology.
Neuroma
,
Acoustic
/ surgery. Treatment Outcome
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(PMID = 16936570.001).
[ISSN]
1531-7129
[Journal-full-title]
Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology
[ISO-abbreviation]
Otol. Neurotol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
51
15.
Miyakawa T, Kamada N, Kobayashi T, Hirano K, Fujii K, Sasahara Y, Nagai Y, Shinkai H:
Neurofibromatosis type 2 in an infant with multiple plexiform schwannomas as first symptom.
J Dermatol
; 2007 Jan;34(1):60-4
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[Title]
Neurofibromatosis type
2 in an infant with multiple plexiform schwannomas as first symptom.
Neurofibromatosis type
2 (
NF2
) is an autosomal dominant
disorder
that is caused by inactivating mutations or a loss of both alleles in the
NF2
tumor-suppressor gene.
Bilateral
vestibular
schwannomas are considered to be the hallmark of this
disease
, with hearing loss and tinnitus which are caused by these tumors, usually presenting as the initial symptoms.
In addition to other tumors and ocular findings, skin abnormalities also occur in
NF2
, however, they are not so characteristic as
neurofibromatosis type
1 (NF1).
We herein report a case of
NF2
which occurred in a 5-year-old boy.
He had multiple cutaneous tumors but did not have any symptoms related to
vestibular
schwannomas.
A histopathological examination revealed these tumors to be plexiform schwannomas; we therefore suspected
NF2
.
As a result of magnetic resonance imaging with gadolinium enhancement,
bilateral
vestibular
schwannomas were detected and a final
diagnosis
of
NF2
was thus made.
The association between
NF2
and multiple depigmented spots is unknown, we therefore consider that multiple cutaneous plexiform schwannomas may strongly suggest an association with
NF2
.
[MeSH-major]
Neurilemmoma / pathology.
Neurofibromatosis 2
/ pathology. Skin Neoplasms / pathology
[MeSH-minor]
Child, Preschool. Humans. Male.
Neuroma
,
Acoustic
/ pathology
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.
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(PMID = 17204104.001).
[ISSN]
0385-2407
[Journal-full-title]
The Journal of dermatology
[ISO-abbreviation]
J. Dermatol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
16.
Kuo YH, Roos D, Brophy BP:
Linear accelerator radiosurgery for treatment of vestibular schwannomas in neurofibromatosis 2.
J Clin Neurosci
; 2008 Jul;15(7):744-8
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[Title]
Linear accelerator radiosurgery for treatment of
vestibular
schwannomas in
neurofibromatosis 2
.
Management of
vestibular
schwannomas in patients with
neurofibromatosis 2
(
NF2
) balances growth control against preservation of hearing with the primary aim of maintaining patient quality of life.
Previous studies on the efficacy of stereotactic radiosurgery for
vestibular
schwannomas in
NF2
have reported results from delivery by Gamma Knife systems.
Modelling studies suggest that lesional conformality is superior with Gamma Knife, but clinical studies on sporadic
vestibular
schwannomas show equivalent results between the two systems.
Our experience with LINAC radiosurgery in
NF2
reported here shows good long-term growth control in four patients with
vestibular
schwannomas.
[MeSH-major]
Neurofibromatosis 2
/ surgery.
Neuroma
,
Acoustic
/ surgery. Radiosurgery / statistics & numerical data
[MeSH-minor]
Adult. Brain Stem / pathology. Brain Stem / physiopathology. Brain Stem / surgery. Deafness / etiology. Deafness / physiopathology. Female. Humans. Magnetic Resonance Imaging. Male. Postoperative Complications / etiology. Postoperative Complications / physiopathology. Retrospective Studies. Treatment Outcome.
Vestibular
Nerve / pathology.
Vestibular
Nerve / physiopathology.
Vestibular
Nerve / radiation effects
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.
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(PMID = 18403208.001).
[ISSN]
0967-5868
[Journal-full-title]
Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
[ISO-abbreviation]
J Clin Neurosci
[Language]
eng
[Publication-type]
Case Reports; Comparative Study; Journal Article
[Publication-country]
Scotland
17.
Buccoliero AM, Castiglione F, R Degl'Innocenti D, Gheri CF, Garbini F, Taddei A, Ammannati F, Mennonna P, Taddei GL:
NF2 gene expression in sporadic meningiomas: relation to grades or histotypes real time-pCR study.
Neuropathology
; 2007 Feb;27(1):36-42
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[Title]
NF2
gene expression in sporadic meningiomas: relation to grades or histotypes real time-pCR study.
One of the most common regions involved in the meningiomas tumorigenesis is chromosome 22q where the
NF2
gene resides.
The deficiency or loss of the
NF2
gene product, merlin/schwannomin, plays a role in tumor development and metastatization.
Several studies have indicated
NF2
gene inactivation as an early tumorigenic event unrelated to the histological grade or clinical behavior.
On the contrary, the
NF2
gene alteration rate differs between the different histotypes.
A pathogenesis independent from the
NF2
gene has been suggested in meningothelial meningiomas.
In the present work, we studied the
NF2
gene expression through real time-PCR (RT-PCR) in 30 meningiomas.
The average of the
NF2
gene expression of all meningiomas was considered as reference value.
The average of expression of WHO grade I and
II
meningiomas was higher than the average of all meningiomas, whereas that of WHO grade III meningiomas was lower.
When we compared the
NF2
gene expression in the different meningioma grades we did not note a significant difference (P = 0.698) despite the tendency to decrease from grade I to grade III.
The difference in
NF2
gene expression between meningothelial and non-meningothelial meningiomas was statistically significant (P = 0.013).
Our data supports the
finding
that alterations in
NF2
gene alteration are histotype related but not grade related.
[MeSH-major]
Genes,
Neurofibromatosis 2
. Meningeal Neoplasms / genetics. Meningeal Neoplasms / pathology. Meningioma / genetics
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(PMID = 17319281.001).
[ISSN]
0919-6544
[Journal-full-title]
Neuropathology : official journal of the Japanese Society of Neuropathology
[ISO-abbreviation]
Neuropathology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Australia
18.
Lomas J, Bello MJ, Arjona D, Alonso ME, Martinez-Glez V, Lopez-Marin I, Amiñoso C, de Campos JM, Isla A, Vaquero J, Rey JA:
Genetic and epigenetic alteration of the NF2 gene in sporadic meningiomas.
Genes Chromosomes Cancer
; 2005 Mar;42(3):314-9
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[Title]
Genetic and epigenetic alteration of the
NF2
gene in sporadic meningiomas.
The role of the
NF2
gene in the development of meningiomas has recently been documented; inactivating mutations plus allelic loss at 22q, the site of this gene (at 22q12), have been identified in both sporadic and
neurofibromatosis type
2-associated tumors.
Although epigenetic inactivation through aberrant CpG island methylation of the
NF2
5' flanking region has been documented in
schwannoma
(another
NF2
-associated neoplasm), data on participation of this epigenetic modification in meningiomas are not yet widely available.
Using methylation-specific PCR (MSP) plus sequencing, we assessed the presence of aberrant promoter
NF2
methylation in a series of 88 meningiomas (61 grade I, 24 grade
II
, and 3 grade III), in which the allelic constitution at 22q and the
NF2
mutational status also were determined by RFLP/microsatellite and PCR-SSCP analyses.
Chromosome 22 allelic loss,
NF2
gene mutation, and aberrant
NF2
promoter methylation were detected in 49%, 24%, and 26% of cases, respectively.
Aberrant
NF2
methylation with loss of heterozygosity (LOH) at 22q was found in five cases, and aberrant methylation with
NF2
mutation in another; LOH 22q and the mutation were found in 16 samples.
The aberrant methylation of the
NF2
gene also was the sole alteration in 15 samples, most of which were from grade I tumors.
These results indicate that aberrant
NF2
hypermethylation may participate in the development of a significant proportion of sporadic meningiomas, primarily those of grade I.
[MeSH-major]
Chromosome Aberrations. Chromosomes, Human, Pair 22. Genes,
Neurofibromatosis 2
/ physiology. Meningeal Neoplasms / genetics. Meningioma / genetics
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(PMID = 15609345.001).
[ISSN]
1045-2257
[Journal-full-title]
Genes, chromosomes & cancer
[ISO-abbreviation]
Genes Chromosomes Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
19.
Dalgliesh GL, Furge K, Greenman C, Chen L, Bignell G, Butler A, Davies H, Edkins S, Hardy C, Latimer C, Teague J, Andrews J, Barthorpe S, Beare D, Buck G, Campbell PJ, Forbes S, Jia M, Jones D, Knott H, Kok CY, Lau KW, Leroy C, Lin ML, McBride DJ, Maddison M, Maguire S, McLay K, Menzies A, Mironenko T, Mulderrig L, Mudie L, O'Meara S, Pleasance E, Rajasingham A, Shepherd R, Smith R, Stebbings L, Stephens P, Tang G, Tarpey PS, Turrell K, Dykema KJ, Khoo SK, Petillo D, Wondergem B, Anema J, Kahnoski RJ, Teh BT, Stratton MR, Futreal PA:
Systematic sequencing of renal carcinoma reveals inactivation of histone modifying genes.
Nature
; 2010 Jan 21;463(7279):360-3
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Furthermore,
NF2
mutations were found in non-VHL mutated ccRCC, and several other probable cancer genes were identified.
These results indicate that substantial genetic heterogeneity exists in a cancer
type
dominated by mutations in a single gene, and that systematic screens will be key to fully determining the somatic genetic architecture of cancer.
[MeSH-major]
Carcinoma, Renal Cell / genetics. Genes,
Neurofibromatosis 2
. Histone-Lysine N-Methyltransferase / genetics. Histones / metabolism. Kidney Neoplasms / genetics. Nuclear Proteins / genetics. Oxidoreductases, N-Demethylating / genetics
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[CommentIn]
Future Oncol. 2010 Jun;6(6):897-900
[
20528227.001
]
(PMID = 20054297.001).
[ISSN]
1476-4687
[Journal-full-title]
Nature
[ISO-abbreviation]
Nature
[Language]
eng
[Databank-accession-numbers]
GEO/ GSE17895
[Grant]
United Kingdom / Wellcome Trust / / 077012/Z/05/Z; United Kingdom / Wellcome Trust / / 082359; United Kingdom / Wellcome Trust / / 088340; United Kingdom / Wellcome Trust / / 093867; United Kingdom / Wellcome Trust / / 077012
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Chromatin; 0 / Histones; 0 / Nuclear Proteins; EC 1.14.11.- / Histone Demethylases; EC 1.14.11.- / KDM5C protein, human; EC 1.14.11.- / UTX protein, human; EC 1.5.- / Oxidoreductases, N-Demethylating; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Set2 protein, human
[Other-IDs]
NLM/ PMC2820242; NLM/ UKMS28099
20.
Hennigan RF, Foster LA, Chaiken MF, Mani T, Gomes MM, Herr AB, Ip W:
Fluorescence resonance energy transfer analysis of merlin conformational changes.
Mol Cell Biol
; 2010 Jan;30(1):54-67
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Neurofibromatosis type
2 is an inherited autosomal
disorder
caused by biallelic inactivation of the
NF2
tumor suppressor gene.
The
NF2
gene encodes a 70-kDa protein, merlin, which is a member of the ezrin-radixin-moesin (ERM) family.
Using these tools, we find that merlin exists predominately as a monomer in a stable, closed conformation that is mediated by the
central
alpha-helical domain.
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Mouse Genome Informatics (MGI)
.
NCI CPTC Antibody Characterization Program.
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.
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[ISSN]
1098-5549
[Journal-full-title]
Molecular and cellular biology
[ISO-abbreviation]
Mol. Cell. Biol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA078524; United States / NCI NIH HHS / CA / R01-CA78524
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Neurofibromin 2; 0 / Phosphoproteins; 0 / Sodium-Hydrogen Antiporter; 0 / sodium-hydrogen exchanger regulatory factor
[Other-IDs]
NLM/ PMC2798298
21.
Sakai T, Vallejo MC, Shannon KT:
A parturient with neurofibromatosis type 2: anesthetic and obstetric considerations for delivery.
Int J Obstet Anesth
; 2005 Oct;14(4):332-5
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[Title]
A parturient with
neurofibromatosis type
2: anesthetic and obstetric considerations for delivery.
Neurofibromatosis type
2 is an extremely rare form of
neurofibromatosis
characterized by
central
nervous system involvement with
bilateral
vestibular
schwannomas and spinal tumors.
Anesthetic management of a parturient with
neurofibromatosis type
2 has not been fully reported, and the condition is challenging to obstetric anesthesiologists due to the presence of intracranial and intraspinal canal neurofibromas.
We present a case of
neurofibromatosis type
2 referred for delivery.
Because of
central
neuraxial involvement, regional anesthesia was avoided, and the patient delivered by cesarean section under general anesthesia.
The importance of pre-operative
diagnosis
and multidisciplinary management for
neurofibromatosis type
2 is emphasized and anesthetic and obstetric considerations for delivery are presented.
[MeSH-major]
Anesthesia, General. Anesthesia, Obstetrical.
Central
Nervous System Neoplasms. Cesarean Section.
Neurofibromatosis 2
. Pregnancy Complications, Neoplastic
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[CommentIn]
Int J Obstet Anesth. 2005 Oct;14(4):277-8
[
16154340.001
]
(PMID = 16140520.001).
[ISSN]
0959-289X
[Journal-full-title]
International journal of obstetric anesthesia
[ISO-abbreviation]
Int J Obstet Anesth
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Netherlands
22.
Plouin PF, Gimenez-Roqueplo AP:
Initial work-up and long-term follow-up in patients with phaeochromocytomas and paragangliomas.
Best Pract Res Clin Endocrinol Metab
; 2006 Sep;20(3):421-34
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Phaeochromocytomas and paragangliomas may be sporadic or the result of several genetic diseases: multiple endocrine neoplasia
type 2
,
neurofibromatosis
1, von Hippel-Lindau
disease
, succinate dehydrogenase-phaeochromocytoma-paraganglioma syndrome.
Familial
cases are diagnosed earlier and are more frequently
bilateral
and recurrent than sporadic cases.
Patients should be followed up indefinitely, particularly if they have
familial
or extra-adrenal tumours.
[MeSH-major]
Paraganglioma / complications. Paraganglioma /
diagnosis
. Pheochromocytoma / complications. Pheochromocytoma /
diagnosis
[MeSH-minor]
Adrenal Gland Neoplasms / complications. Adrenal Gland Neoplasms /
diagnosis
. Adrenal Gland Neoplasms / radiography. Adrenal Gland Neoplasms / radionuclide imaging. Aftercare. Algorithms. Diagnostic Imaging. Follow-Up Studies. Humans. Perioperative Care. Prognosis
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(PMID = 16980203.001).
[ISSN]
1521-690X
[Journal-full-title]
Best practice & research. Clinical endocrinology & metabolism
[ISO-abbreviation]
Best Pract. Res. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Number-of-references]
70
23.
Ogasawara N, Sasaki M, Ishiguro H, Itoh Y, Nojiri S, Kubota E, Wada T, Kataoka H, Kuwabara Y, Joh T:
Gastric schwannoma with adjacent external progression harbored aberrant NF2 gene.
Dig Endosc
; 2009 Jul;21(3):192-5
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[Title]
Gastric
schwannoma
with adjacent external progression harbored aberrant
NF2
gene.
We describe
a schwannoma
of gastric origin with adjacent external progression.
Histology and immunohistochemistry revealed the typical appearance of a gastric
schwannoma
.
Genetic evaluation revealed that the tumor harbored a point mutation in exon 6 of the tumor suppressor
neurofibromatosis 2
(
NF2
) gene, which resulted in an amino acid substitution of
NF2
protein, and no mutation in exon 4b of the NF1 gene.
In conclusion, we identified a rare mutation of the
NF2
gene in gastric
schwannoma
.
A diagnosis
can only be definitive when based on histological and immunohistochemical findings.
[MeSH-major]
Neurilemmoma / genetics.
Neurofibromatosis 2
/ genetics. Stomach Neoplasms / genetics
[MeSH-minor]
Disease
Progression. Female. Humans. Middle Aged
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(PMID = 19691769.001).
[ISSN]
1443-1661
[Journal-full-title]
Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society
[ISO-abbreviation]
Dig Endosc
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Australia
24.
Mathieu D, Kondziolka D, Flickinger JC, Niranjan A, Williamson R, Martin JJ, Lunsford LD:
Stereotactic radiosurgery for vestibular schwannomas in patients with neurofibromatosis type 2: an analysis of tumor control, complications, and hearing preservation rates.
Neurosurgery
; 2007 Mar;60(3):460-8; discussion 468-70
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[Title]
Stereotactic radiosurgery for
vestibular
schwannomas in patients with
neurofibromatosis type
2: an analysis of tumor control, complications, and hearing preservation rates.
OBJECTIVE:
Vestibular
schwannomas present significant management challenges in patients with
neurofibromatosis Type
2 (
NF2
).
Facial neuropathy occurred in 8% of tumors, trigeminal neuropathy occurred in 4%, and
vestibular
dysfunction occurred in 4%.
CONCLUSION: Stereotactic radiosurgery is a safe and effective management modality for
neurofibromatosis Type 2 vestibular
schwannomas.
[MeSH-major]
Hearing Loss, Sensorineural / epidemiology. Hearing Loss, Sensorineural / prevention & control. Neurilemmoma / epidemiology. Neurilemmoma / surgery.
Neurofibromatosis 2
/ epidemiology.
Neurofibromatosis 2
/ surgery. Radiosurgery / statistics & numerical data
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(PMID = 17327790.001).
[ISSN]
1524-4040
[Journal-full-title]
Neurosurgery
[ISO-abbreviation]
Neurosurgery
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
United States
25.
Suárez C, Rodrigo JP, Ferlito A, Cabanillas R, Shaha AR, Rinaldo A:
Tumours of familial origin in the head and neck.
Oral Oncol
; 2006 Nov;42(10):965-78
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[Title]
Tumours of
familial
origin in the head and neck.
Tumours of
familial
origin are a rare event in the head and neck but despite this, they deserve a growing interest.
Familial
paragangliomas are most of the time limited to the paraganglionar system, but also may be part of different syndromic associations.
Multiple endocrine neoplasias
type
1 are characterized by the simultaneous occurrence of at least two of the three main related endocrine tumours: parathyroid, enteropancreatic and anterior pituitary.
Multiple endocrine neoplasia
type 2
is due to a germline mutation in the RET proto-oncogene.
The most
central
clinical difference with MEN-1 is that the associated cancer can be prevented or cured by early thyroidectomy in mutation carriers.
Individuals with neurofibomatosis
type
1 present early in life with pigmentary abnormalities, skinfold freckling and iris hamartomas, as result of NF1 gene mutation.
Neurofibromatosis 2
is caused by inactivating mutations of the
NF2
gene, and is characterized by the development of nervous system tumours (mainly
bilateral
vestibular
schwannomas), ocular abnormalities, and skin tumours.
Finally, the high rate of p16 mutations in squamous cell carcinomas and the association of p16 with
familial
melanoma propose p16 as an ideal candidate gene predisposing to
familial
squamous cell carcinomas.
The elucidation of the cellular processes affected by dysfunction in
familial
tumours of the head and neck may serve to identify potential targets for future therapeutic interventions.
[MeSH-minor]
Carcinoma, Squamous Cell / genetics. Humans. Multiple Endocrine Neoplasia / genetics. Nasopharyngeal Neoplasms / genetics.
Neurofibromatoses
/ genetics. Paraganglioma / genetics
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(PMID = 16857415.001).
[ISSN]
1368-8375
[Journal-full-title]
Oral oncology
[ISO-abbreviation]
Oral Oncol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Number-of-references]
121
26.
Siddiqui MA, Leslie T, Scott C, Mackenzie J:
Eyelid schwannoma in a male adult.
Clin Exp Ophthalmol
; 2005 Aug;33(4):412-3
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[Title]
Eyelid
schwannoma
in a male adult.
Solitary lesions can occur sporadically in the general population but multiple neurofibromas are distinctive feature of
neurofibromatosis type
1 and
bilateral acoustic
schwannomas are a feature of
neurofibromatosis type
2.
Herein, a case of eyelid
schwannoma
in a 53-year-old man is described.
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(PMID = 16033357.001).
[ISSN]
1442-6404
[Journal-full-title]
Clinical & experimental ophthalmology
[ISO-abbreviation]
Clin. Experiment. Ophthalmol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Australia
27.
Walter J, Kuhn SA, Brodhun M, Reichart R, Kalff R:
Pulmonary meningioma and neurinoma associated with multiple CNS tumours in a patient with neurofibromatosis type 2.
Clin Neurol Neurosurg
; 2009 Jun;111(5):454-9
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[Title]
Pulmonary meningioma and neurinoma associated with multiple CNS tumours in a patient with
neurofibromatosis type
2.
OBJECTIVE:
Neurofibromatosis type
2 (
NF2
) is a common neurocutaneous
disorder
that exhibits an autosomal dominant inheritance, with a mutation at chromosome 22q12.2.
In general, patients present
bilateral
vestibular
schwannomas, meningiomas and neurinomas of the
central
and peripheral nervous system as well as neurofibromas and gliomas.
There is no reported case of pulmonary meningiomas and neurinomas associated with
NF2
until now.
PATIENT AND METHODS: Here, we present a 16-year-old girl with
NF
-2 associated to CNS and pulmonary tumours and we discuss the case in the backlight of the literature.
RESULTS: The reported patient presented
a de
novo
NF2
germline mutation (R341X) and displayed the Wishart-
type
of
NF
-2 since she is 11 years old, with a huge anaplastic biparietal falx meningioma and a tentorium meningioma and a tumour-associated parietal mass as well as hypacusis starting at the infant age of 3 years.
CONCLUSION: This rare case extends our knowledge of
NF2
and also raises interesting questions about the pathogenesis of meningiomas outside the CNS.
[MeSH-major]
Central
Nervous System Neoplasms / pathology. Lung Neoplasms / secondary. Meningioma / secondary.
Neurofibromatosis 2
/ complications
[MeSH-minor]
Brain / radiography. Brain Edema. Child. Female. Genes,
Neurofibromatosis 2
/ physiology. Germ-Line Mutation. Humans. Lung / pathology. Magnetic Resonance Imaging. Tomography, X-Ray Computed
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(PMID = 19249154.001).
[ISSN]
1872-6968
[Journal-full-title]
Clinical neurology and neurosurgery
[ISO-abbreviation]
Clin Neurol Neurosurg
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Netherlands
28.
Lau YK, Murray LB, Houshmandi SS, Xu Y, Gutmann DH, Yu Q:
Merlin is a potent inhibitor of glioma growth.
Cancer Res
; 2008 Jul 15;68(14):5733-42
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Neurofibromatosis 2
(
NF2
) is an inherited cancer syndrome in which affected individuals develop nervous system tumors, including schwannomas, meningiomas, and ependymomas.
The
NF2
protein merlin (or schwannomin) is a member of the Band 4.1 superfamily of proteins, which serve as linkers between transmembrane proteins and the actin cytoskeleton.
In addition to mutational inactivation of the
NF2
gene in
NF2
-associated tumors, mutations and loss of merlin expression have also been reported in other types of cancers.
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Mol Cancer Ther. 2006 Mar;5(3):494-501
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]
(PMID = 18632626.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / 1F32CA128335-01A1; United States / NCI NIH HHS / CA / CA135158-02; United States / NCI NIH HHS / CA / R01 CA135158-02; United States / NCI NIH HHS / CA / CA135158-01A1; United States / NCI NIH HHS / CA / F32 CA128335; United States / NCI NIH HHS / CA / R01 CA135158-01A1; United States / NCI NIH HHS / CA / R01 CA135158; United States / NCI NIH HHS / CA / R01 CA150355
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Neurofibromin 2; 0 / Wnt Proteins
[Other-IDs]
NLM/ NIHMS147652; NLM/ PMC2778036
29.
Jeblaoui Y, Neji B, Haddad S, Mnif D, Hchicha S:
[Difficulties of the management of head and neck neurofibromatosis].
Ann Chir Plast Esthet
; 2007 Feb;52(1):43-50
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[Title]
[Difficulties of the management of head and neck
neurofibromatosis
].
[Transliterated title]
Difficultés
de
la prise en charge des atteintes
de
l'extrémité céphalique dans les
neurofibromatoses
.
INTRODUCTION:
Neurofibromatoses
represent a group of 7 diseases having the same cutaneous signs due to a common embryologic origin.
Neurofibromatosis type
1 (NF1) or Von Recklinghausen's
neurofibromatosis
is an autosomal dominantly inherited
disease
, whose prevalence is 1/4500.
Neurofibromatosis type
2 (
NF2
) is also an autosomal dominantly inherited
disease
, but is ten times less frequent than the NF1 and is characterized by
bilateral
vestibular
schwannomas (former
acoustic
neurinomas).
Eight patients were found carrier of NF1 and one patient carrier of
NF2
according to the diagnostic criteria of the 1988's National Institute of Health consensus.
The patient having
NF2
was treated by neurosurgery and showed a good result.
Facial
neurofibromatoses
are difficult to control given the presence of soft tissues infiltration and the associated osseous dysplasia.
Cancer risks and the
disease
's completely unpredictable evolution urge a regular and multidisciplinary patient follow-up.
[MeSH-major]
Head and Neck Neoplasms / surgery.
Neurofibromatosis
1 / surgery.
Neurofibromatosis 2
/ surgery
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(PMID = 17137698.001).
[ISSN]
0294-1260
[Journal-full-title]
Annales de chirurgie plastique et esthétique
[ISO-abbreviation]
Ann Chir Plast Esthet
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
30.
James MF, Han S, Polizzano C, Plotkin SR, Manning BD, Stemmer-Rachamimov AO, Gusella JF, Ramesh V:
NF2/merlin is a novel negative regulator of mTOR complex 1, and activation of mTORC1 is associated with meningioma and schwannoma growth.
Mol Cell Biol
; 2009 Aug;29(15):4250-61
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[Title]
NF2
/merlin is a novel negative regulator of mTOR complex 1, and activation of mTORC1 is associated with meningioma and
schwannoma
growth.
Inactivating mutations of the
neurofibromatosis 2
(
NF2
) gene,
NF2
, result predominantly in benign neurological tumors, schwannomas and meningiomas, in humans; however, mutations in murine
Nf2
lead to a broad spectrum of cancerous tumors.
The tumor-suppressive function of the
NF2
protein, merlin, a membrane-cytoskeleton linker, remains unclear.
NF2
patient tumors and
Nf2
-deficient mouse embryonic fibroblasts demonstrate elevated mTORC1 signaling.
Conversely, the exogenous expression of wild-
type
merlin isoforms, but not a patient-derived L64P mutant, suppresses mTORC1 signaling.
In conclusion, the deregulation of mTORC1 activation underlies the aberrant growth and proliferation of
NF2
-associated tumors and may restrain the growth of these lesions through negative feedback mechanisms, suggesting that rapamycin in combination with phosphoinositide 3-kinase inhibitors may be therapeutic for
NF2
.
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(PMID = 19451225.001).
[ISSN]
1098-5549
[Journal-full-title]
Molecular and cellular biology
[ISO-abbreviation]
Mol. Cell. Biol.
[Language]
ENG
[Grant]
United States / NINDS NIH HHS / NS / P30 NS045776; United States / NINDS NIH HHS / NS / NS 045776; United States / NIMH NIH HHS / MH / R21 MH079213; United States / NIMH NIH HHS / MH / MH 079213; United States / NINDS NIH HHS / NS / P01 NS024279; United States / NCI NIH HHS / CA / R01 CA122617-04; United States / NINDS NIH HHS / NS / NS 024279; United States / NCI NIH HHS / CA / CA122617-04; United States / NCI NIH HHS / CA / R01 CA122617
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibiotics, Antineoplastic; 0 / Multiprotein Complexes; 0 / Neurofibromin 2; 0 / Proteins; 0 / RNA, Small Interfering; 0 / Transcription Factors; 0 / mechanistic target of rapamycin complex 1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; W36ZG6FT64 / Sirolimus
[Other-IDs]
NLM/ PMC2715803
31.
Hanemann CO, Bartelt-Kirbach B, Diebold R, Kämpchen K, Langmesser S, Utermark T:
Differential gene expression between human schwannoma and control Schwann cells.
Neuropathol Appl Neurobiol
; 2006 Dec;32(6):605-14
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[Title]
Differential gene expression between human
schwannoma
and control Schwann cells.
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.
As the events leading to
schwannoma
development are largely unknown we investigated the differences in gene expression between
schwannoma
cells from
NF2
patients and normal human primary Schwann cells by cDNA array analysis.
By this method a total of seven genes with increased and seven genes with decreased mRNA levels in
schwannoma
compared with normal Schwann cells could be identified.
[MeSH-major]
Gene Expression. Neurilemmoma / genetics.
Neurofibromatosis 2
/ genetics. Schwann Cells / physiology
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(PMID = 17083475.001).
[ISSN]
0305-1846
[Journal-full-title]
Neuropathology and applied neurobiology
[ISO-abbreviation]
Neuropathol. Appl. Neurobiol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / RNA, Messenger
32.
Cotticelli L, Romano M, Russo S, Borrelli M:
Neurofibromatosis type 2: a case of ptosis.
Graefes Arch Clin Exp Ophthalmol
; 2007 Sep;245(9):1393-6
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[Title]
Neurofibromatosis type
2: a case of ptosis.
BACKGROUND:
Neurofibromatosis type
2 (
NF2
) is
a disorder
usually diagnosed later in life since the features are subtle in children.
The hallmark is
bilateral
vestibular
schwannomas, which may not appear until after the second decade.
Here is described a rare case of
NF2
associated with a superior rectus muscle paralysis and severe ptosis.
CASE REPORT: A 17-year-old patient with
NF2
was referred to us with
diagnosis
of left-eye superior rectus muscle paralysis, with a later onset of unilateral severe ptosis.
The patient showed positive
familiar
history for
NF
(the father was affected),
bilateral
involvement of the
acoustic
nerves (
schwannoma
), multiple neurofibromas, and
bilateral
posterior subcapsular lens opacity.
Magnetic resonance imaging (MRI) showed
bilateral acoustic
neuromas in the left temporal region close to the cavernous sinus; since neurological examination and ocular motility problems had remained stationary over time, surgical correction of ptosis and strabismus was suggested.
CONCLUSION: Palpebral ptosis has rarely been reported in
NF2
.
[MeSH-major]
Blepharoptosis / complications.
Neurofibromatosis 2
/ complications. Oculomotor Muscles / pathology. Ophthalmoplegia / complications
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[Cites]
Br J Ophthalmol. 1993 Oct;77(10):662-72
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8218038.001
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Curr Opin Neurol. 2003 Feb;16(1):27-33
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[
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]
[Cites]
Am J Med Genet. 1994 Oct 1;52(4):450-61
[
7747758.001
]
(PMID = 17347811.001).
[ISSN]
0721-832X
[Journal-full-title]
Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie
[ISO-abbreviation]
Graefes Arch. Clin. Exp. Ophthalmol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
33.
Rowe J, Grainger A, Walton L, Radatz M, Kemeny A:
Safety of radiosurgery applied to conditions with abnormal tumor suppressor genes.
Neurosurgery
; 2007 May;60(5):860-4; discussion 860-4
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OBJECTIVE: To assess the risk of radiosurgery inducing malignancy in
neurofibromatosis
-2 (
NF2
) and von Hippel-Lindau
disease
.
METHODS: A retrospective cohort study of 118
NF2
and 19 von Hippel-Lindau
disease
patients, totalling 906 and 62 patient-years of follow-up data, respectively.
RESULTS: Two cases of intracranial malignancy were identified, both of which occurred in
NF2
patients.
CONCLUSION: Because gliomas may occur in as many as 4% of
NF2
patients, this may not represent an increased risk.
We continue to offer radiosurgery treatment to selected
NF2
and von Hippel-Lindau
disease
patients and consider that the late risk of malignancy arising after irradiation must be put in the context of the condition being treated, the treatment options available to these individuals, and their life expectancy.
[MeSH-minor]
Adult. Cohort Studies. Female. Follow-Up Studies. Humans. Male. Middle Aged.
Neurofibromatosis 2
/ epidemiology.
Neurofibromatosis 2
/ genetics.
Neurofibromatosis 2
/ surgery. Retrospective Studies. von Hippel-Lindau
Disease
/ epidemiology. von Hippel-Lindau
Disease
/ genetics. von Hippel-Lindau
Disease
/ surgery
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(PMID = 17460521.001).
[ISSN]
1524-4040
[Journal-full-title]
Neurosurgery
[ISO-abbreviation]
Neurosurgery
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
34.
Dereure O:
[Molecular characterisation of SMARCB1 and NF2 in familial and sporadic schwannomatosis: an evolving paradigm].
Ann Dermatol Venereol
; 2008 Dec;135(12):888-9
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[Title]
[Molecular characterisation of SMARCB1 and
NF2
in
familial
and sporadic schwannomatosis: an evolving paradigm].
[Transliterated title]
Caractérisation moléculaire
de
SMARCB1 et
NF2
dans la schwannomatose familiale et sporadique : un paradigme qui évolue.
[MeSH-major]
Chromosomal Proteins, Non-Histone. DNA-Binding Proteins. Neurilemmoma / genetics.
Neurofibromatosis 2
/ genetics. Transcription Factors
[MeSH-minor]
Animals. Chromosomes, Human, Pair 22 / genetics.
Disease
Models, Animal. Humans. Mice. Mutation
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(PMID = 19084709.001).
[ISSN]
0151-9638
[Journal-full-title]
Annales de dermatologie et de vénéréologie
[ISO-abbreviation]
Ann Dermatol Venereol
[Language]
fre
[Publication-type]
Journal Article
[Publication-country]
France
[Chemical-registry-number]
0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / SMARCB1 protein, human; 0 / Transcription Factors
35.
Bosch MM, Mironov A, Killer HE:
Atypical manifestation of neurofibromatosis type 2 in a boy.
Eye (Lond)
; 2005 Jun;19(6):705-6
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[Title]
Atypical manifestation of
neurofibromatosis type
2 in a boy.
[MeSH-major]
Cataract /
diagnosis
. Cranial Nerve Neoplasms /
diagnosis
. Neurilemmoma /
diagnosis
.
Neurofibromatosis 2
/
diagnosis
. Trigeminal Nerve Diseases /
diagnosis
[MeSH-minor]
Child. Codon, Nonsense. Genes,
Neurofibromatosis 2
. Humans. Male
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.
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consumer health - Neurofibromatosis type 2
.
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.
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(PMID = 15192694.001).
[ISSN]
0950-222X
[Journal-full-title]
Eye (London, England)
[ISO-abbreviation]
Eye (Lond)
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
[Chemical-registry-number]
0 / Codon, Nonsense
36.
Bouccara D, Kalamarides M, Bozorg Grayeli A, Ambert-Dahan E, Rey A, Sterkers O:
[Auditory brainstem implant: indications and results].
Ann Otolaryngol Chir Cervicofac
; 2007 Jul;124(3):148-54
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OBJECTIVES: To summarize the indications and evaluate the Auditory Brainstem Implant (ABI) performances in
neurofibromatosis type
2 (
NF2
) and other otologics indications, as postmeningitis ossified cochlea.
MATERIAL AND METHODS: Main and first indication of ABI is
NF2
.
Emergent indications are
bilateral
total ossified cochlea,
vestibular schwannoma
with controlateral lesions, cochlear nerve aplasia or inner ear's malformations.
RESULTS: In
NF2
patients, best results are obtained in cases of smaller
vestibular schwannoma
and none, or short term, auditory deprivation.
CONCLUSION: These results show a clear benefit of ABI in
NF2
patients, with or without previous tumor removal, in case of small tumor with a short duration of hearing loss.
[MeSH-minor]
Brain / pathology. Calcinosis / etiology. Calcinosis / pathology. Cochlear Diseases / etiology. Cochlear Diseases / pathology. Cochlear Nerve / pathology. Cochlear Nerve / surgery. Electrodes, Implanted. Female. Humans. Magnetic Resonance Imaging. Middle Aged.
Neurofibromatosis 2
/ complications.
Neuroma
,
Acoustic
/ complications.
Neuroma
,
Acoustic
/ pathology.
Neuroma
,
Acoustic
/ surgery
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(PMID = 17320034.001).
[ISSN]
0003-438X
[Journal-full-title]
Annales d'oto-laryngologie et de chirurgie cervico faciale : bulletin de la Société d'oto-laryngologie des hôpitaux de Paris
[ISO-abbreviation]
Ann Otolaryngol Chir Cervicofac
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
37.
Seong MW, Yeo IK, Cho SI, Park CK, Kim SK, Paek SH, Kim DG, Jung HW, Park H, Kim SY, Kim JY, Park SS:
Molecular characterization of the NF2 gene in Korean patients with neurofibromatosis type 2: a report of four novel mutations.
Korean J Lab Med
; 2010 Apr;30(2):190-4
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[Title]
Molecular characterization of the
NF2
gene in Korean patients with
neurofibromatosis type
2: a report of four novel mutations.
BACKGROUND:
Neurofibromatosis type
2 (
NF2
) is an autosomal dominant syndrome caused by the
NF2
tumor suppressor gene.
However, the
NF2
mutation characteristics in Korean patients are not sufficiently understood.
In this study, we conducted a comprehensive mutational analysis in 7 Korean
NF2
patients by performing direct sequencing and gene-dosage assessment.
METHODS: We analyzed all exons and flanking regions of
NF2
by direct sequencing and screened the deletions or duplications involving
NF2
by multiplex ligation-dependent probe amplification.
RESULTS: Four novel
NF2
mutations, including 2 splice-site mutations (c.364-1G>A and c.886-3C>G), 1 frameshift mutation (c.524delA), and 1 missense mutation (c.397T>C; p.Cys133Arg), were identified in our patients.
CONCLUSIONS: The detection rate of
NF2
mutations in Korean patients (57%) is similar to those in other populations.
Our results provided a greater insight into the mutational spectrum of the
NF2
gene in Korean subjects.
[MeSH-major]
Asian Continental Ancestry Group / genetics. Genes,
Neurofibromatosis 2
. Mutation.
Neurofibromatosis 2
/ genetics
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(PMID = 20445339.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / RNA Splice Sites
38.
Rennie AT, Side L, Kerr RS, Anslow P, Pretorius P:
Intramedullary tumours in patients with neurofibromatosis type 2: MRI features associated with a favourable prognosis.
Clin Radiol
; 2008 Feb;63(2):193-200
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[Title]
Intramedullary tumours in patients with
neurofibromatosis type
2: MRI features associated with a favourable prognosis.
AIM: To assess the magnetic resonance imaging (MRI) features and natural history of intramedullary tumours in patients with
neurofibromatosis type
2 (
NF2
).
MATERIALS AND METHODS: Eleven
NF2
patients with intramedullary spinal cord tumours were identified from the database of the multidisciplinary
NF2
clinic.
CONCLUSION: The majority of intramedullary tumours in
NF2
patients are very slow growing and share certain MRI features that differ from those of progressive or symptomatic lesions.
[MeSH-major]
Neurofibromatosis 2
/
diagnosis
.
Neuroma
,
Acoustic
/
diagnosis
. Spinal Cord Neoplasms /
diagnosis
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.
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.
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(PMID = 18194696.001).
[ISSN]
0009-9260
[Journal-full-title]
Clinical radiology
[ISO-abbreviation]
Clin Radiol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Contrast Media
39.
Simon M, Boström JP, Hartmann C:
Molecular genetics of meningiomas: from basic research to potential clinical applications.
Neurosurgery
; 2007 May;60(5):787-98; discussion 787-98
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Mutations in the
NF2
gene probably account for the formation of more than half of all meningiomas.
On the other hand, the molecular events underlying the initiation of meningiomas without
NF2
mutations have yet to be identified.
SciCrunch.
KEGG: Data: Disease Annotation
.
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(PMID = 17460514.001).
[ISSN]
1524-4040
[Journal-full-title]
Neurosurgery
[ISO-abbreviation]
Neurosurgery
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
119
40.
Trotter MI, Briggs RJ:
Cochlear implantation in neurofibromatosis type 2 after radiation therapy.
Otol Neurotol
; 2010 Feb;31(2):216-9
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[Title]
Cochlear implantation in
neurofibromatosis type
2 after radiation therapy.
OBJECTIVE: To investigate the results of cochlear implantation in patients with
neurofibromatosis Type
2 (
NF2
) who have previously been treated with radiation therapy to the
vestibular schwannoma
(VS) in their only hearing ear.
STUDY DESIGN: A retrospective review of the Melbourne Cochlear implant database was undertaken to identify patients with
NF2
undergoing cochlear implantation in whom previous radiation therapy had been performed to control their VS (ipsilateral tumor).
CONCLUSION: Cochlear implantation results in improved hearing in a select group of
NF2
patients who have undergone radiation treatment to control their vs.
[MeSH-major]
Cochlear Implantation.
Neurofibromatosis 2
/ complications.
Neurofibromatosis 2
/ radiotherapy
[MeSH-minor]
Adult. Aged, 80 and over. Communication. Ear Neoplasms / complications. Ear Neoplasms / radiotherapy. Female. Hearing Loss / etiology. Hearing Loss / therapy. Humans. Lipreading. Magnetic Resonance Imaging. Male. Middle Aged.
Neuroma
,
Acoustic
/ complications.
Neuroma
,
Acoustic
/ radiotherapy. Postoperative Complications / therapy. Radiosurgery. Recovery of Function. Retrospective Studies. Speech Perception. Treatment Outcome
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(PMID = 19887974.001).
[ISSN]
1537-4505
[Journal-full-title]
Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology
[ISO-abbreviation]
Otol. Neurotol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
41.
Nakai Y, Zheng Y, MacCollin M, Ratner N:
Temporal control of Rac in Schwann cell-axon interaction is disrupted in NF2-mutant schwannoma cells.
J Neurosci
; 2006 Mar 29;26(13):3390-5
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[Title]
Temporal control of Rac in Schwann cell-axon interaction is disrupted in
NF2
-mutant
schwannoma
cells.
The
neurofibromatosis type
2 (
NF2
) gene is commonly mutated in schwannomas, Schwann cell tumors that contain cells lacking axon interaction.
NF2
is involved in suppression of Rac signaling, and cultured
schwannoma
cells contain elevated, GTP-bound, active Rac.
Despite these previous studies, a causal relationship between Rac activation and the abnormal cellular morphology of
schwannoma
is unknown.
We used fluorescence resonance energy transfer to follow Rac activity in normal human Schwann cells and
schwannoma
cells during interaction with neurons.
Schwannoma
cells showed high Rac activity at distal regions of the cells and failed to align processes with neurites.
Application of a Rac-specific inhibitor, the chemical compound NSC23766, to
schwannoma
cells restored neuronal interaction.
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.
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.
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.
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(PMID = 16571745.001).
[ISSN]
1529-2401
[Journal-full-title]
The Journal of neuroscience : the official journal of the Society for Neuroscience
[ISO-abbreviation]
J. Neurosci.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA118032; United States / NCI NIH HHS / CA / CA75824
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Neurofibromin 2; EC 3.6.5.2 / rac GTP-Binding Proteins
42.
McClatchey AI:
Neurofibromatosis.
Annu Rev Pathol
; 2007;2:191-216
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[Title]
Neurofibromatosis
.
As
familial
cancer syndromes, the
neurofibromatoses
exhibit complex phenotypes, comprising a range of tumor and nontumor manifestations.
Although the three recognized forms of
neurofibromatosis
(NF1,
NF2
, and schwannomatosis) all feature the development of nervous system tumors, their underlying genetic bases are clearly distinct.
Recent progress in delineating the molecular function of the NF1- and
NF2
-encoded proteins, together with the development and use of manipulable mouse models, has led to important advances in understanding the pathogenesis of many features of
neurofibromatosis
.
An important outcome of the study of
neurofibromatosis
-associated tumorigenesis has been insight into the more general molecular and cellular bases of nervous system tumors.
[MeSH-major]
Nervous System Neoplasms / pathology. Neurilemmoma / pathology.
Neurofibromatosis
1 / pathology.
Neurofibromatosis 2
/ pathology
[MeSH-minor]
Animals.
Disease
Models, Animal. Humans. Mice. Neurofibromin 1 / genetics. Neurofibromin 1 / metabolism. Neurofibromin 2 / genetics. Neurofibromin 2 / metabolism. Peripheral Nervous System / metabolism. Peripheral Nervous System / pathology. Schwann Cells / metabolism. Schwann Cells / pathology
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.
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(PMID = 18039098.001).
[ISSN]
1553-4006
[Journal-full-title]
Annual review of pathology
[ISO-abbreviation]
Annu Rev Pathol
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01CA113733-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Neurofibromin 1; 0 / Neurofibromin 2
[Number-of-references]
148
43.
Horan G, Whitfield GA, Burton KE, Burnet NG, Jefferies SJ:
Fractionated conformal radiotherapy in vestibular schwannoma: early results from a single centre.
Clin Oncol (R Coll Radiol)
; 2007 Sep;19(7):517-22
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[Title]
Fractionated conformal radiotherapy in
vestibular schwannoma
: early results from a single centre.
AIMS: To assess the local control and cranial nerve toxicity in
vestibular schwannoma
patients treated with fractionated conformal radiotherapy delivered using a linear accelerator.
There were five
neurofibromatosis type
2 patients treated, two of whom had useful hearing before radiotherapy.
CONCLUSION: Although follow-up was relatively short in this single institution series, fractionated linear accelerator radiotherapy gave excellent local control, useful hearing preservation and retained cranial nerve function in
vestibular schwannoma
.
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Cranial Nerves / radiation effects. Dose Fractionation. Female. Hearing / radiation effects. Humans. Male. Middle Aged.
Neuroma
,
Acoustic
. Stereotaxic Techniques
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(PMID = 17400433.001).
[ISSN]
0936-6555
[Journal-full-title]
Clinical oncology (Royal College of Radiologists (Great Britain))
[ISO-abbreviation]
Clin Oncol (R Coll Radiol)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
44.
Yang SM, Yu LM, Yu LM, Han DY:
[Technique of hearing preservation during acoustic neuroma surgery].
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
; 2008 Aug;43(8):564-9
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[Title]
[Technique of hearing preservation during
acoustic
neuroma
surgery].
OBJECTIVE: To explore the possibility of hearing protection in
acoustic
neurinoma (AN) resection and to evaluate the effect of dynamic auditory monitoring and the effect of oto-endoscope for hearing protection.
Fifteen cases were solitary AN, 3 cases were diagnosed as
neurofibromatosis II
.
RESULTS: In all 18 cases, tumors were resected completely in 16 cases, but sub-totally removed in 2 cases which were
II neurofibromatosis
.
According to House-Brackmann grade system, for 18 AN patients 7 days after operation only 50.0% (9/18) were kept at grade I to
II
, but 88.9% (16/18) were kept at grade I to
II
6 months after operation.
[MeSH-major]
Hearing Loss / prevention & control.
Neuroma
,
Acoustic
/ surgery. Otologic Surgical Procedures
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.
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.
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(PMID = 18959258.001).
[ISSN]
1673-0860
[Journal-full-title]
Zhonghua er bi yan hou tou jing wai ke za zhi = Chinese journal of otorhinolaryngology head and neck surgery
[ISO-abbreviation]
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
45.
Laskin WB, Fetsch JF, Lasota J, Miettinen M:
Benign epithelioid peripheral nerve sheath tumors of the soft tissues: clinicopathologic spectrum of 33 cases.
Am J Surg Pathol
; 2005 Jan;29(1):39-51
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Benign epithelioid peripheral nerve sheath tumors (BEPNSTs) have not been fully characterized, and their relationship to conventional
schwannoma
and neurofibroma has not been satisfactorily established.
Only one patient probably has
neurofibromatosis type
1.
Immunohistochemical reactivity for Schwann cell-related markers in tumor cells included S-100 protein (20 of 20 cases), collagen
type
IV (10 of 10), laminin (8 of 8), nerve growth factor receptor, p75(7 of 8), CD57 (6 of 9), and glial fibrillary acidic protein (8 of 15).
The remaining 15 cases showed some histologic features suggestive of
schwannoma
, but their uniform cellularity, absence of nuclear palisading, and presence of a significant CD34-positive spindled cell population in 5 cases led to their classification as "BEPNST of indeterminate histogenesis."
Evaluation for loss of heterozygosity in 2 cases demonstrated deletion of genetic material on chromosome 22q and 17q involving
NF2
and NF1 loci.
However, sequencing of
NF2
coding sequences revealed no mutations.
Follow-up for 18 patients (median interval, 13.5 years), including 4 patients with tumors exhibiting cytologic atypia, revealed a nondestructive recurrence or persistent
disease
in 3 patients whose tumors lacked atypia, but no evidence of metastatic spread or tumor-related death.
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(PMID = 15613855.001).
[ISSN]
0147-5185
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Neurofibromin 1; 0 / Neurofibromin 2
46.
Al-Anazi AH, Al-Luwimi IM, Shawarby MA, Mertol T:
Mixed vestibular schwannoma and meningioma without neurofibromatosis.
Neurosciences (Riyadh)
; 2009 Oct;14(4):371-3
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[Title]
Mixed
vestibular schwannoma
and meningioma without
neurofibromatosis
.
The co-existence of meningioma and
schwannoma
as 2 distinct histologic components within the same tumor has been described in
neurofibromatosis 2
(
NF2
), but the co-existence of both tumors without evidence of
NF2
is much rarer.
Here, we are reporting a case of mixed
schwannoma
with meningioma without clinical evidence of
NF2
.
In an adult Saudi lady with progressive left-sided hearing loss, left cerebellopontine tumor was diagnosed by MRI, and the histopathological
diagnosis
revealed that this tumor was composed of
vestibular schwannoma
and meningioma.
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(PMID = 21048654.001).
[ISSN]
1319-6138
[Journal-full-title]
Neurosciences (Riyadh, Saudi Arabia)
[ISO-abbreviation]
Neurosciences (Riyadh)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Saudi Arabia
47.
Ng YS, Lyons CJ:
Oculomotor nerve palsy in childhood.
Can J Ophthalmol
; 2005 Oct;40(5):645-53
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BACKGROUND: The management of children with oculomotor nerve palsy is complicated by their variable presentation, amblyopia, potential loss of binocularity, and associated neurological
disease
.
Primary aberrant regeneration was the presenting sign in a child with
neurofibromatosis type
2.
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(PMID = 16391633.001).
[ISSN]
0008-4182
[Journal-full-title]
Canadian journal of ophthalmology. Journal canadien d'ophtalmologie
[ISO-abbreviation]
Can. J. Ophthalmol.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
England
48.
Massager N, Nissim O, Delbrouck C, Devriendt D, David P, Desmedt F, Wikler D, Hassid S, Brotchi J, Levivier M:
Role of intracanalicular volumetric and dosimetric parameters on hearing preservation after vestibular schwannoma radiosurgery.
Int J Radiat Oncol Biol Phys
; 2006 Apr 1;64(5):1331-40
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[Title]
Role of intracanalicular volumetric and dosimetric parameters on hearing preservation after
vestibular schwannoma
radiosurgery.
PURPOSE: To analyze the relationship between hearing preservation after gamma knife radiosurgery (GKR) for
vestibular schwannoma
(VS) and some volumetric and dosimetric parameters of the intracanalicular components of vs. METHODS AND MATERIALS: This study included 82 patients with a VS treated by GKR; all patients had no
NF2 disease
, a Gardner-Robertson hearing class 1-4 before treatment, a marginal dose of 12 Gy, and a radiologic and audiologic follow-up > or =1 year post-GKR.
[MeSH-major]
Neuroma
,
Acoustic
/ surgery. Radiosurgery
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(PMID = 16458446.001).
[ISSN]
0360-3016
[Journal-full-title]
International journal of radiation oncology, biology, physics
[ISO-abbreviation]
Int. J. Radiat. Oncol. Biol. Phys.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
49.
Guntinas-Lichius O:
Hearing improvement after bevacizumab for neurofibromatosis type 2.
N Engl J Med
; 2009 Oct 29;361(18):1809-10; author reply 1810-1
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[Title]
Hearing improvement after bevacizumab for
neurofibromatosis type
2.
[MeSH-major]
Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Hearing Loss / drug therapy.
Neurofibromatosis 2
/ complications.
Neuroma
,
Acoustic
/ drug therapy
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[CommentOn]
N Engl J Med. 2009 Jul 23;361(4):358-67
[
19587327.001
]
(PMID = 19864683.001).
[ISSN]
1533-4406
[Journal-full-title]
The New England journal of medicine
[ISO-abbreviation]
N. Engl. J. Med.
[Language]
eng
[Publication-type]
Comment; Letter
[Publication-country]
United States
[Chemical-registry-number]
0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab
50.
Jaurand MC, Fleury-Feith J:
Pathogenesis of malignant pleural mesothelioma.
Respirology
; 2005 Jan;10(1):2-8
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Genetic alterations in the tumour suppressor genes, P16/CDKN2A and
neurofibromatosis 2
(
NF2
), are found both in human MPM and in asbestos-exposed
Nf2
-deficient mice.
Despite a ban on asbestos use in Western countries, the incidence of MPM is increasing, due to the long delay between asbestos exposure and
diagnosis
.
[MeSH-minor]
Animals. Asbestosis / complications. Cell Transformation, Neoplastic / pathology. Cocarcinogenesis. Genes,
Neurofibromatosis 2
. Genes, Tumor Suppressor. Humans. Mice. Polyomavirus Infections / complications. Simian virus 40. Tumor Virus Infections / complications
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(PMID = 15691231.001).
[ISSN]
1323-7799
[Journal-full-title]
Respirology (Carlton, Vic.)
[ISO-abbreviation]
Respirology
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Australia
[Number-of-references]
68
51.
Retrosi G, Nanni L, Ricci R, Manzoni C, Pintus C:
Plexiform schwannoma of the esophagus in a child with neurofibromatosis type 2.
J Pediatr Surg
; 2009 Jul;44(7):1458-61
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[Title]
Plexiform
schwannoma
of the esophagus in a child with
neurofibromatosis type
2.
Schwannoma
is a benign neoplasia of the peripheral nerve sheath.
According to the existing literature esophageal
schwannoma
has been reported so far only in adult patients.
We report the case of an 11 year old patient with
neurofibromatosis
,
type 2
, who underwent surgical excision of a plexiform
schwannoma
of the esophagus.
[MeSH-major]
Esophageal Neoplasms /
diagnosis
. Esophagectomy / methods. Neoplasms, Multiple Primary. Neurilemmoma /
diagnosis
.
Neurofibromatosis 2
/
diagnosis
[MeSH-minor]
Child.
Diagnosis
, Differential. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Tomography, X-Ray Computed
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(PMID = 19573680.001).
[ISSN]
1531-5037
[Journal-full-title]
Journal of pediatric surgery
[ISO-abbreviation]
J. Pediatr. Surg.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
52.
Jatana KR, Jacob A, Slone HW, Ray-Chaudhury A, Welling DB:
Spinal myxopapillary ependymoma metastatic to bilateral internal auditory canals.
Ann Otol Rhinol Laryngol
; 2008 Feb;117(2):98-102
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[Title]
Spinal myxopapillary ependymoma metastatic to
bilateral
internal auditory canals.
OBJECTIVES: We report a rare case of spinal myxopapillary ependymoma metastatic to both internal auditory canals (IACs) and its implications for diagnosing
neurofibromatosis type
2 (
NF2
).
METHODS: We present a detailed clinical history, magnetic resonance imaging (MRI), intraoperative photographs, and histopathologic findings from a patient with
bilateral
IAC lesions, and review the diagnostic criteria for
NF2
.
The
diagnosis
of
NF2
with
bilateral
vestibular
schwannomas was entertained.
This
finding
raised the possibility of other, more unusual IAC lesions.
The patient underwent sequential suboccipital craniotomies for tissue
diagnosis
, and both IAC lesions were found to be myxopapillary ependymomas.
Although
vestibular
schwannomas account for the majority of contrast-enhancing T1-weighted IAC lesions, other uncommon lesions may present in a similar manner.
Therefore, both T1-weighted MRI with or without contrast and T2-weighted MRI may be necessary to distinguish
vestibular schwannoma
from other, more unusual IAC lesions.
[MeSH-major]
Ear Neoplasms /
diagnosis
. Ear Neoplasms / secondary. Ependymoma /
diagnosis
. Ependymoma / secondary. Labyrinth Diseases /
diagnosis
. Spinal Cord Neoplasms / pathology
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(PMID = 18357830.001).
[ISSN]
0003-4894
[Journal-full-title]
The Annals of otology, rhinology, and laryngology
[ISO-abbreviation]
Ann. Otol. Rhinol. Laryngol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
53.
Soos S, Balasko M, Jech-Mihalffy A, Szekely M, Petervari E:
Anorexic vs. metabolic effects of central leptin infusion in rats of various ages and nutritional states.
J Mol Neurosci
; 2010 May;41(1):97-104
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[Title]
Anorexic vs. metabolic effects of
central
leptin infusion in rats of various ages and nutritional states.
In the present experiments, the anorexic (suppressing food intake and body weight) and hypermetabolic (increasing body temperature (Tc), activity, and heart rate (HR), indicating metabolic rate) responses to 7-day-long intracerebroventricular leptin infusion were compared in 2- and 6-month-old normally fed (
NF2
and NF6 groups), 6-month-old high-fat-diet-induced obese (HF6), and 6-month-old calorie-restricted (CR6) rats.
The anorexic effects were inversely related to fat content: They were most pronounced in
NF2
, less in NF6, non-significant in HF6 rats, but also absent in CR6 animals of the lowest fat content.
In contrast, CR6 rats were hypersensitive to the metabolic effects of leptin infusion (rise in Tc and HR; biotelemetric measurements),
NF2
were still sensitive, while NF6 and HF6 rats exhibited moderate or low sensitivity.
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[ISSN]
1559-1166
[Journal-full-title]
Journal of molecular neuroscience : MN
[ISO-abbreviation]
J. Mol. Neurosci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Dietary Fats; 0 / Leptin
54.
O'Brien DF, Farrell M, Pidgeon CN:
Combined nasal and skull base pathology: adjacent nasal schwannoma and olfactory groove meningioma.
Br J Neurosurg
; 2005 Oct;19(5):446-8
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[Title]
Combined nasal and skull base pathology: adjacent nasal
schwannoma
and olfactory groove meningioma.
Following surgical removal of the lesion histopathology confirmed the presence of both a nasal
schwannoma
and an olfactory groove meningioma.
This dual pathology may represent a variation of
neurofibromatosis type
2 (
NF
-2).
[MeSH-major]
Meningioma /
diagnosis
. Neoplasms, Multiple Primary /
diagnosis
. Neurilemmoma /
diagnosis
. Nose Neoplasms /
diagnosis
. Skull Base Neoplasms /
diagnosis
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(PMID = 16455571.001).
[ISSN]
0268-8697
[Journal-full-title]
British journal of neurosurgery
[ISO-abbreviation]
Br J Neurosurg
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
55.
Kameswaran M, Vasudevan MC, Kumar RS, Nagasundaram J, Natarajan K, Raghunandhan S:
Auditory brainstem implantation: The first Indian experience.
Indian J Otolaryngol Head Neck Surg
; 2005 Jan;57(1):58-63
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Multichannel auditory brainstem implants (ABI) are currently indicated for patients with
neurofibromatosis type II
(
NF2
) involving both vestibulocochlear nerves.
The implant is usually placed in the
lateral
recess of the fourth ventricle at the time of tumor resection to stimulate the cochlear nucleus.
We report a case of ABI done on a 15-year-old girl with
bilateral
vestibular
schwannomas.
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[Cites]
J Laryngol Otol Suppl. 2000;(27):11-4
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11211429.001
]
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[ISSN]
2231-3796
[Journal-full-title]
Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India
[ISO-abbreviation]
Indian J Otolaryngol Head Neck Surg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Other-IDs]
NLM/ PMC3451539
[Keywords]
NOTNLM ; auditory brainsterm unplants / neurofibromatosis
56.
Chow HY, Stepanova D, Koch J, Chernoff J:
p21-Activated kinases are required for transformation in a cell-based model of neurofibromatosis type 2.
PLoS One
; 2010 Nov 02;5(11):e13791
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[Title]
p21-Activated kinases are required for transformation in a cell-based model of
neurofibromatosis type
2.
BACKGROUND:
NF2
is an autosomal dominant
disease
characterized by development of
bilateral
vestibular
schwannomas and other benign tumors in
central
nervous system.
Loss of the
NF2
gene product, Merlin, leads to aberrant Schwann cell proliferation, motility, and survival, but the mechanisms by which this tumor suppressor functions remain unclear.
CONCLUSIONS/SIGNIFICANCE: These results suggest that Pak functions in novel signaling pathways in
NF2
, and may serve as a useful therapeutic target in this
disease
.
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.
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[
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[
19451229.001
]
[Cites]
Mol Cell. 2010 Apr 23;38(2):236-49
[
20417602.001
]
(PMID = 21072183.001).
[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA006927; United States / NCI NIH HHS / CA / R01 CA117884; United States / NCI NIH HHS / CA / CA117884
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Neurofibromin 2; EC 2.7.11.1 / p21-Activated Kinases
[Other-IDs]
NLM/ PMC2970553
57.
Łaniewski-Wołłk M, Gos M, Koziarski A, Szpecht-Potocka A:
Identification of mutations in the NF2 gene in Polish patients with neurofibromatosis type 2.
J Appl Genet
; 2008;49(3):297-300
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[Title]
Identification of mutations in the
NF2
gene in Polish patients with
neurofibromatosis type
2.
Point mutation and loss of heterozygosity (LOH) analyses were performed in 12 Polish patients with a classic symptom of
NF2
-
bilateral
vestibular
schwannomas (BVS).
In 5 patients (41.7%), germline mutations were found in the
NF2
gene: 2 previously reported substitutions (c.592C>T and c.52C>T) and 3 novel mutations (c.1001_1002insG, c.1029_1030insCC, c.774_778dupGAATG).
In addition, LOH analysis of 30 tumour samples from 10 patients revealed a molecular basis of
NF2
in 3 patients (25%) that did not have any germline mutation.
The molecular defects in sporadic cases of
NF2
are still being discussed.
[MeSH-major]
Germ-Line Mutation / genetics. Loss of Heterozygosity.
Neurofibromatosis 2
/ genetics
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[ISSN]
1234-1983
[Journal-full-title]
Journal of applied genetics
[ISO-abbreviation]
J. Appl. Genet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
58.
Nakamura E, Kaelin WG Jr:
Recent insights into the molecular pathogenesis of pheochromocytoma and paraganglioma.
Endocr Pathol
; 2006;17(2):97-106
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These tumors can arise in the context of hereditary cancer syndromes such as von Hippel- Lindau
disease
, multiple endocrine neoplasia
type 2
, and
neurofibromatosis
1.
This review focuses on the genetics of these tumors and suggests a possible link between
familial
pheochromocytomas/paraganglioma genes and control of neuronal apoptosis during embryological development.
[MeSH-major]
Adrenal Gland Neoplasms / genetics. Fetal Development / physiology. Genetic Predisposition to
Disease
. Paraganglioma / genetics. Pheochromocytoma / genetics
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[ISSN]
1046-3976
[Journal-full-title]
Endocrine pathology
[ISO-abbreviation]
Endocr. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
9061-61-4 / Nerve Growth Factor; EC 1.3.99.1 / Succinate Dehydrogenase
[Number-of-references]
63
59.
Xiao HJ, Au DK, Yau H, Chow CK, Fan YW, Wei WI:
Neurofibromatosis type 2 and auditory brainstem implantation.
Chin Med J (Engl)
; 2007 Aug 20;120(16):1456-9
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[Title]
Neurofibromatosis type
2 and auditory brainstem implantation.
[MeSH-major]
Auditory Brain Stem Implantation / methods.
Neurofibromatosis 2
/ surgery
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(PMID = 17825179.001).
[ISSN]
0366-6999
[Journal-full-title]
Chinese medical journal
[ISO-abbreviation]
Chin. Med. J.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
China
60.
Baser ME, Rai H, Wallace AJ, Evans DG:
Neurofibromatosis 2 (NF2) and malignant mesothelioma in a man with a constitutional NF2 missense mutation.
Fam Cancer
; 2005;4(4):321-2
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[Title]
Neurofibromatosis 2
(
NF2
) and malignant mesothelioma in a man with a constitutional
NF2
missense mutation.
Neurofibromatosis 2
(
NF2
) is caused by inactivating mutations of the
NF2
tumor suppressor gene.
Somatic
NF2
mutations also occur in a high proportion of human primary malignant mesotheliomas.
We report an elderly man with
NF2
, malignant mesothelioma, and a constitutional
NF2
missense mutation.
The long latent period for mesothelioma in this patient (61 years) raises the possibility that the
type
of mutant
NF2
allele could affect mesothelioma tumorigenesis or progression.
[MeSH-major]
Genes,
Neurofibromatosis 2
. Mesothelioma / complications. Mesothelioma / genetics.
Neurofibromatosis 2
/ genetics. Occupational Exposure / adverse effects. Pleural Neoplasms / genetics
[MeSH-minor]
Aged. Asbestos / adverse effects. Humans. Male. Mutation, Missense.
Neuroma
,
Acoustic
/ etiology. Polymerase Chain Reaction
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Clinical Genomic Database: Data: Gene Annotation
.
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1389-9600
[Journal-full-title]
Familial cancer
[ISO-abbreviation]
Fam. Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Netherlands
[Chemical-registry-number]
1332-21-4 / Asbestos
61.
Stamenkovic I, Yu Q:
Merlin, a "magic" linker between extracellular cues and intracellular signaling pathways that regulate cell motility, proliferation, and survival.
Curr Protein Pept Sci
; 2010 Sep;11(6):471-84
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Genetic alterations of
neurofibromatosis type
2 (
NF2
) gene lead to the development of schwannomas, meningiomas, and ependymomas.
Mutations of
NF2
gene were also found in thyroid cancer, mesothelioma, and melanoma, suggesting that it functions as a tumor suppressor in a wide spectrum of cells.
The product of
NF2
gene is merlin (moesin-ezrin-radixin-like protein), a member of the Band 4.1 superfamily proteins.
Accumulating data also suggested an emerging role of merlin as a negative regulator of growth and progression of several non-
NF2
associated cancer types.
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(PMID = 20491622.001).
[ISSN]
1875-5550
[Journal-full-title]
Current protein & peptide science
[ISO-abbreviation]
Curr. Protein Pept. Sci.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA135158-02; United States / NCI NIH HHS / CA / R01 CA135158-02; United States / NCI NIH HHS / CA / CA150355-01A1; United States / NCI NIH HHS / CA / R01 CA150355-01A1; United States / NCI NIH HHS / CA / 1R01CA150355-01A1; United States / NCI NIH HHS / CA / R01 CA135158; United States / NCI NIH HHS / CA / R01 CA150355; United States / NCI NIH HHS / CA / 1R01CA135158-01A1
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Neurofibromin 2
[Other-IDs]
NLM/ NIHMS236013; NLM/ PMC2946555
62.
Galcheva-Gargova Z, Zhidkova N, Geisler S, Ozug J, Wudyka S, Gunay NS, Qi YW, Shriver Z, Venkataraman G:
Overexpression of Merlin in B16F10 mouse melanoma cells reduces their metastatic activity: role of the cell surface heparan sulfate glycosaminoglycans.
Int J Oncol
; 2008 Jun;32(6):1237-43
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Merlin, the protein product of the
neurofibromatosis type
2 gene (
NF2
) acts as a tumor suppressor in mice and humans.
In this study, melanoma B16F10 cells were engineered to overexpress the
NF2
gene by establishing stable transductants.
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(PMID = 18497985.001).
[ISSN]
1019-6439
[Journal-full-title]
International journal of oncology
[ISO-abbreviation]
Int. J. Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Neurofibromin 2; 9050-30-0 / Heparitin Sulfate
63.
Utermark T, Kaempchen K, Antoniadis G, Hanemann CO:
Reduced apoptosis rates in human schwannomas.
Brain Pathol
; 2005 Jan;15(1):17-22
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Schwannomas, tumors originating from Schwann cells, represent a frequent neurological tumor and can occur both in a genetic
disorder
called
neurofibromatosis type
2 (
NF2
) and sporadically.
In both cases the genetic background is identical as all schwannomas are caused by biallelic mutations in the tumor suppressor gene
NF2
coding for merlin.
Mutations in this gene have also been found to be responsible for 50% to 60% of spontaneous and 100% of the
NF2
associated meningiomas.
The
NF2
gene product, merlin, links transmembrane proteins to the cytoskeleton and is involved in intracellular signaling processes.
It has previously been shown that reexpression of wild-
type
merlin in primary human
schwannoma
cells leads to an increase in the number of apoptotic cells.
Here, we report in vivo and in vitro evidence that the basal apoptosis rate of primary human
schwannoma
cells is reduced in comparison to that of normal Schwann cells, supporting the idea that in this benign tumor
type
, apoptosis has a role in tumorigenesis.
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(PMID = 15779232.001).
[ISSN]
1015-6305
[Journal-full-title]
Brain pathology (Zurich, Switzerland)
[ISO-abbreviation]
Brain Pathol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
64.
Bhatoe HS, Singh P, Dutta V:
Intraventricular meningiomas: a clinicopathological study and review.
Neurosurg Focus
; 2006;20(3):E9
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METHODS: In this retrospective analysis, the authors describe the cases of 12 patients who had received
a diagnosis
of intraventricular meningioma and underwent surgery for the tumors.
Features of
neurofibromatosis Type
2 were present in two of the women.
Nine of the tumors were located in the
lateral
ventricles, one was in the third ventricle, and two were in the fourth ventricle.
Excision was performed using the parietooccipital (trigonal) approach for
lateral
ventricle tumors, the transcortical-transventricular route for the third ventricle tumor, and suboccipital craniectomy for fourth ventricle tumors.
Although they are commonly seen in the
lateral
ventricles, they occur in the third and fourth ventricles as well.
Presentation is in the form of raised ICP with no localizing features; therefore the
diagnosis
is based on imaging studies.
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(PMID = 16599425.001).
[ISSN]
1092-0684
[Journal-full-title]
Neurosurgical focus
[ISO-abbreviation]
Neurosurg Focus
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
26
65.
Akinci A, Acaroglu G, Guven A, Degerliyurt A:
Refractive errors in neurofibromatosis type 1 and type 2.
Br J Ophthalmol
; 2007 Jun;91(6):746-8
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[Title]
Refractive errors in
neurofibromatosis type
1 and
type 2
.
OBJECTIVE: To document the prevalence of refractive errors in patients with
neurofibromatosis type
1 (NF1) and
type 2
(
NF2
) and to compare it with that of age- and sex-matched controls.
METHODS: 82 patients with NF1, 21 patients with
NF2
and 103 age- and sex-matched controls were evaluated in this prospective observational case-control study.
RESULTS: The prevalence of myopia was 23.1% in patients with NF1, 23.8% in patients with
NF2
and 16.5% in age- and sex-matched controls.
These differences were significant (p<0.03, p<0.03), and adjusting for intelligence, education, height, weight and BMI increased the significance of this
finding
(p<0.001, p<0.001).
CONCLUSION: A high prevalence of myopia seems to be an additional feature of NF1 and
NF2
.
[MeSH-major]
Neurofibromatosis
1 / complications.
Neurofibromatosis 2
/ complications. Refractive Errors / etiology
Genetic Alliance.
consumer health - Neurofibromatosis
.
Genetic Alliance.
consumer health - Neurofibromatosis type 1
.
Genetic Alliance.
consumer health - Neurofibromatosis type 2
.
MedlinePlus Health Information.
consumer health - Refractive Errors
.
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]
(PMID = 17202204.001).
[ISSN]
0007-1161
[Journal-full-title]
The British journal of ophthalmology
[ISO-abbreviation]
Br J Ophthalmol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC1955624
66.
Zuccala' A, Di Nicolo' P, Fiorenza S, Lifrieri F, Rapana' R:
[The sympathetic system and neuroendocrine hypertension].
G Ital Nefrol
; 2008 Mar-Apr;25(2):203-14
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Sporadic pheochromocytoma is a rare tumor that should be taken into account in patients with hypertensive crisis, arrhythmias, and panic
disorder
.
Familial
pheochromocytoma is frequently found in subjects with von Hippel-Lindau
disease
, multiple endocrine neoplasia
type II
,
neurofibromatosis
, and SDHD gene mutations.
Plasma free metanephrines have been shown to have high sensitivity and specificity in the biochemical
diagnosis
of sporadic and
familial
pheochromocytoma.
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(PMID = 18350500.001).
[ISSN]
0393-5590
[Journal-full-title]
Giornale italiano di nefrologia : organo ufficiale della Società italiana di nefrologia
[ISO-abbreviation]
G Ital Nefrol
[Language]
ita
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Italy
[Number-of-references]
49
67.
Evans DG, Maher ER, Baser ME:
Age related shift in the mutation spectra of germline and somatic NF2 mutations: hypothetical role of DNA repair mechanisms.
J Med Genet
; 2005 Aug;42(8):630-2
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[Title]
Age related shift in the mutation spectra of germline and somatic
NF2
mutations: hypothetical role of DNA repair mechanisms.
We compared the ratio of frameshift to nonsense mutations in three diseases that are related to the
NF2
tumour suppressor gene: classic
neurofibromatosis 2
(
NF2
), caused by germline
NF2
mutations; mosaic
NF2
; and unilateral sporadic
vestibular schwannoma
(USVS), caused by somatic
NF2
inactivation.
Nonsense mutations predominated in both classic and mosaic
NF2
, but the ratio of nonsense to frameshift mutations was reversed in USvs. Moreover, in USVS patients, the ratio of somatic frameshift to nonsense mutations increased significantly with increasing age at
diagnosis
.
Similar studies for other
familial
cancer genes may provide further evidence for this hypothesis.
[MeSH-major]
Codon, Nonsense. DNA Repair / physiology. Frameshift Mutation. Genes,
Neurofibromatosis 2
. Germ-Line Mutation
[MeSH-minor]
Age Factors. Genetic Predisposition to
Disease
. Humans. Mosaicism.
Neuroma
,
Acoustic
/ genetics
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[Cites]
Am J Hum Genet. 2000 Jan;66(1):84-91
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10631138.001
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Environ Mol Mutagen. 2000;36(4):301-11
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Cancer Res. 2001 Oct 1;61(19):6991-5
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Mol Cell Biol. 2001 Nov;21(22):7587-600
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Cancer. 2001 Dec 1;92(11):2920-6
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Ann N Y Acad Sci. 2001 Apr;928:113-20
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]
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Mol Cell Biol. 2002 Apr;22(7):2410-8
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Mutat Res. 2002 Mar 20;500(1-2):135-45
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Gene. 2002 May 1;289(1-2):41-8
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Mech Ageing Dev. 2002 Apr 30;123(8):907-15
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[
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]
[Cites]
Mutat Res. 2000 Apr 28;459(3):195-202
[
10812331.001
]
(PMID = 16061561.001).
[ISSN]
1468-6244
[Journal-full-title]
Journal of medical genetics
[ISO-abbreviation]
J. Med. Genet.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Codon, Nonsense
[Other-IDs]
NLM/ PMC1736122
68.
Franzin A, Spatola G, Serra C, Picozzi P, Medone M, Milani D, Castellazzi P, Mortini P:
Evaluation of hearing function after Gamma Knife surgery of vestibular schwannomas.
Neurosurg Focus
; 2009 Dec;27(6):E3
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[Title]
Evaluation of hearing function after Gamma Knife surgery of
vestibular
schwannomas.
OBJECT: Due to technological advances in neuroradiology in recent years, incidental diagnoses of
vestibular
schwannomas (VSs) have increased.
METHODS: Of all patients treated in the authors' hospital between 2001 and 2007, they retrospectively studied 50 patients with a unilateral VS in whom there was serviceable hearing (Gardner-Robertson [GR] Class I or
II
).
Additional inclusion criteria were: no
Type 2 neurofibromatosis
, no previous treatment, and at least 6 months' follow-up of neuroradiological and audiological data.
Serviceable hearing was preserved in 34 patients (68%): 21 (62%) with GR Class I hearing and 13 (38%) with GR Class
II
hearing.
In 19 (58%) of 33 patients with GR Class I function before GKS the same class was maintained posttreatment; 29 (88%) maintained functional hearing (GR Class I or
II
).
Significant prognostic factors for maintaining serviceable hearing were GR Class I function before treatment, symptoms at presentation, patient age younger than 54 years, and Koos Stage T1
disease
.
The prescribed dose of 13 Gy appears to represent an excellent compromise between controlling the
disease
and preserving auditory function.
[MeSH-major]
Hearing Loss / prevention & control.
Neuroma
,
Acoustic
/ surgery. Postoperative Complications / prevention & control. Radiosurgery / methods
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(PMID = 19951056.001).
[ISSN]
1092-0684
[Journal-full-title]
Neurosurgical focus
[ISO-abbreviation]
Neurosurg Focus
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
69.
Yu H, Ye L, Mansel RE, Zhang Y, Jiang WG:
Clinical implications of the influence of Ehm2 on the aggressiveness of breast cancer cells through regulation of matrix metalloproteinase-9 expression.
Mol Cancer Res
; 2010 Nov;8(11):1501-12
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Ehm2, a member of
NF2
/ERM/4.1 superfamily, has been indicated in
disease
progression and metastasis of prostate cancer.
Higher levels of Ehm2 transcripts were correlated with
disease
progression, metastasis, and poor prognosis.
Disease
-free survival of the patients with lower levels of Ehm2 was 135.8 (95% confidence interval, 125.1-146.5) months, significantly longer compared with 102.5 (95% confidence interval, 78.7-126.4) months of patients with higher levels of Ehm2 expression (P = 0.039).
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[Copyright]
©2010 AACR.
(PMID = 21047774.001).
[ISSN]
1557-3125
[Journal-full-title]
Molecular cancer research : MCR
[ISO-abbreviation]
Mol. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Cytoskeletal Proteins; 0 / EPB41L4B protein, human; 0 / RNA, Catalytic; 0 / hammerhead ribozyme; EC 3.4.24.35 / Matrix Metalloproteinase 9
70.
Mazzoni A, Dubey SP, Poletti AM, Colombo G:
Sporadic acoustic neuroma in pediatric patients.
Int J Pediatr Otorhinolaryngol
; 2007 Oct;71(10):1569-72
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[Title]
Sporadic
acoustic
neuroma
in pediatric patients.
OBJECTIVE: Sporadic
acoustic
neuroma
, usually occur between the ages of 40 and 70 years, are very rare in children.
We review the experiences of 10 cases of sporadic (non-
NF2
)
acoustic
neuromas in pediatric patients.
Among these almost 900 cases were
acoustic
neuromas.
Postoperatively seven cases the facial nerve recovered to grade I, and one each to grade
II
and grade VI of House-Brackmann classification.
[MeSH-major]
Neuroma
,
Acoustic
/ epidemiology
[MeSH-minor]
Adolescent. Adult. Child. Child, Preschool. Female. Hearing Loss, Sensorineural /
diagnosis
. Hearing Loss, Sensorineural / epidemiology. Humans. Incidence. Male. Paresis /
diagnosis
. Paresis / epidemiology. Paresis / etiology. Postoperative Complications. Prevalence. Tomography, X-Ray Computed
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.
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(PMID = 17643497.001).
[ISSN]
0165-5876
[Journal-full-title]
International journal of pediatric otorhinolaryngology
[ISO-abbreviation]
Int. J. Pediatr. Otorhinolaryngol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Ireland
71.
Martinez-Glez V, Bello MJ, Franco-Hernandez C, De Campos JM, Isla A, Vaquero J, Rey JA:
Mutational analysis of the DAL-1/4.1B tumour-suppressor gene locus in meningiomas.
Int J Mol Med
; 2005 Oct;16(4):771-4
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The DAL-1/41B gene (differentially expressed in adenocarcinoma of the lung), located in the chromosome 18p11.3 region, belongs to the protein family 4.1 (membrane-associated proteins), which includes the product of the
NF2
gene (merlin), and the proteins, ezrin, radixin, and moesin.
We found the following sequence variations; Ala555Thr (G1663A in exon 13) and Thr950Lys (C2849A in exon 19) in two cases each, and one case with a 5pb deletion (
del
taaaa) in intron 18.
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(PMID = 16142420.001).
[ISSN]
1107-3756
[Journal-full-title]
International journal of molecular medicine
[ISO-abbreviation]
Int. J. Mol. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / DNA, Neoplasm; 0 / EPB41L3 protein, human; 0 / Membrane Proteins; 0 / Microfilament Proteins; 0 / Tumor Suppressor Proteins
72.
Bosch MM, Wichmann WW, Boltshauser E, Landau K:
Optic nerve sheath meningiomas in patients with neurofibromatosis type 2.
Arch Ophthalmol
; 2006 Mar;124(3):379-85
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[Title]
Optic nerve sheath meningiomas in patients with
neurofibromatosis type
2.
OBJECTIVE: To determine the prevalence of optic nerve sheath meningiomas (ONSMs) in patients with
neurofibromatosis type
2 (
NF2
).
METHODS: An observational retrospective case series of 30 consecutive patients with
NF2
referred to an academic ophthalmology unit from November 1, 1991, through August 31, 2003.
Diagnosis
of ONSM was made based on typical neuroradiologic and clinical features in 7 patients and on histologic criteria in 1.
RESULTS: Eight of 30 patients harbored unilateral (n = 6) or
bilateral
(n = 2) ONSMs.
CONCLUSIONS: There is a strong association between ONSMs and
NF2
that parallels the well-known association of optic nerve gliomas with NF1.
Physicians should be aware of the possibility that patients with ONSMs may also have
NF2
.
[MeSH-major]
Meningioma /
diagnosis
.
Neurofibromatosis 2
/
diagnosis
. Optic Nerve Neoplasms /
diagnosis
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(PMID = 16534058.001).
[ISSN]
0003-9950
[Journal-full-title]
Archives of ophthalmology (Chicago, Ill. : 1960)
[ISO-abbreviation]
Arch. Ophthalmol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
73.
Ruggieri M, Iannetti P, Polizzi A, La Mantia I, Spalice A, Giliberto O, Platania N, Gabriele AL, Albanese V, Pavone L:
Earliest clinical manifestations and natural history of neurofibromatosis type 2 (NF2) in childhood: a study of 24 patients.
Neuropediatrics
; 2005 Feb;36(1):21-34
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[Title]
Earliest clinical manifestations and natural history of
neurofibromatosis type
2 (
NF2
) in childhood: a study of 24 patients.
BACKGROUND:
Neurofibromatosis type
2 (
NF2
) is an autosomal dominant
disease
characterised by the development of multiple nervous system tumours, ocular abnormalities, and skin tumours.
Although classically considered
a disease
of adults, initial signs and/or symptoms may be evident in childhood and are often unrecognised.
OBJECTIVES: The aim of this study was to identify the earliest clinical presentations of
NF2
and to characterise the clinical course and outcome in children with
NF2
.
METHODS: We have performed a retrospective (years 1990-1998) and prospective (years 1998-2004) study of 24 patients (10 males, 14 females; currently aged 4 to 22 years) fulfilling the revised (Manchester)
NF2
criteria seen at the Universities of Catania and Rome, Italy.
RESULTS: Causes of referral prior to a definitive
diagnosis
of
NF2
were:.
3) Neurological dysfunction: seizures secondary to intracranial meningioma (n = 1) or
vestibular
schwannomas (VS) (n = 1), neurological dysfunction related to brainstem and/or spinal cord tumours (n = 7), isolated and multiple cranial nerve deficits (n = 10), and peripheral neuropathy secondary to schwannomas (n = 4);.
Molecular genetic analysis of the
NF2
gene revealed typical truncating mutations in all the 5
familial
cases and in 2/10 sporadic cases analysed.
CONCLUSIONS: Children with
NF2
often first come to medical attention because of ocular, subtle skin, or neurological problems the significance of which is realised when they later present with more classical symptoms due to
bilateral
VS or other intracranial tumours.
[MeSH-major]
Neurofibromatosis 2
/ physiopathology. Otorhinolaryngologic Diseases / etiology
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(PMID = 15776319.001).
[ISSN]
0174-304X
[Journal-full-title]
Neuropediatrics
[ISO-abbreviation]
Neuropediatrics
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Germany
74.
Patil S, Perry A, Maccollin M, Dong S, Betensky RA, Yeh TH, Gutmann DH, Stemmer-Rachamimov AO:
Immunohistochemical analysis supports a role for INI1/SMARCB1 in hereditary forms of schwannomas, but not in solitary, sporadic schwannomas.
Brain Pathol
; 2008 Oct;18(4):517-9
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The INI1/SMARCB1 protein product (INI1), a component of a transcription complex, was recently implicated in the pathogenesis of schwannomas in two members of a single family with
familial
schwannomatosis.
To determine if this
finding
could be extended to all tumors arising in
familial
schwannomatosis, and how it compares with other multiple
schwannoma
syndromes [sporadic schwannomatosis and
neurofibromatosis 2
(
NF2
)] as well as to sporadic, solitary schwannomas, we performed an immunohistochemistry analysis on 45 schwannomas from patients with multiple
schwannoma
syndromes and on 38 solitary, sporadic schwannomas from non-syndromic patients.
A mosaic pattern of INI1 expression was seen in 93% of tumors from
familial
schwannomatosis patients, 55% of tumors from sporadic schwannomatosis, 83% of
NF2
-associated tumors and only 5% of solitary, sporadic schwannomas.
These results confirm a role for INI1/SMARCB1 in multiple
schwannoma
syndromes and suggest that a different pathway of tumorigenesis occurs in solitary, sporadic tumors.
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[Cites]
Oncogene. 2001 May 28;20(24):3067-75
[
11420722.001
]
[Cites]
Neurology. 2003 Jun 24;60(12):1968-74
[
12821741.001
]
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Neurology. 2005 Jun 14;64(11):1838-45
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]
[Cites]
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]
[Cites]
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[
16528370.001
]
[Cites]
Pediatr Blood Cancer. 2006 Sep;47(3):279-84
[
16261613.001
]
[Cites]
Am J Hum Genet. 1997 Dec;61(6):1293-302
[
9399891.001
]
(PMID = 18422762.001).
[ISSN]
1015-6305
[Journal-full-title]
Brain pathology (Zurich, Switzerland)
[ISO-abbreviation]
Brain Pathol.
[Language]
ENG
[Grant]
United States / NINDS NIH HHS / NS / NS024279-20A29010; United States / NINDS NIH HHS / NS / P01 NS024279-20A29010
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / Genetic Markers; 0 / Neurofibromin 2; 0 / SMARCB1 protein, human; 0 / Transcription Factors
[Other-IDs]
NLM/ NIHMS114873; NLM/ PMC2743242
75.
Zhao ZS, Manser E:
Do PAKs make good drug targets?
F1000 Biol Rep
; 2010;2:70
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The genetic loss of
NF2
(
neurofibromatosis type
2) leading to increased cell proliferation through a Ras-Rac-PAK pathway may represent a good test system to analyze this new PAK inhibitor.
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(PMID = 21173843.001).
[ISSN]
1757-594X
[Journal-full-title]
F1000 biology reports
[ISO-abbreviation]
F1000 Biol Rep
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC2989626
76.
Michalowski MB, de Fraipont F, Michelland S, Entz-Werle N, Grill J, Pasquier B, Favrot MC, Plantaz D:
Methylation of RASSF1A and TRAIL pathway-related genes is frequent in childhood intracranial ependymomas and benign choroid plexus papilloma.
Cancer Genet Cytogenet
; 2006 Apr 1;166(1):74-81
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Ependymomas (EP) represent the third most frequent
type
of
central
nervous system (CNS) tumor of childhood, after astrocytomas and medulloblastomas.
The present objective was, for a sample of 27 children with intracranial EP and 7 with CPP, to describe and compare the methylation status of 19 genes (with current HUGO symbol, if any): p15INK4a (CDKN2B), p16INK4a and p14ARF (both CDKN2A), APC, RB1, RASSF1A (RASSF1), BLU (ZMYND10) FHIT, RARB, MGMT, DAPK (DAPK1), ECAD (CDH1), CASP8, TNFRSF10C, TNFRSF10D, FLIP (CFLAR), INI1 (SMARCB1), TIMP3, and
NF2
.
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(PMID = 16616114.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / RASSF1 protein, human; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Proteins
77.
Holland K, Kaye AH:
Spinal tumors in neurofibromatosis-2: management considerations - a review.
J Clin Neurosci
; 2009 Feb;16(2):169-77
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[Title]
Spinal tumors in
neurofibromatosis
-2: management considerations - a review.
Neurofibromatosis Type
2 (
NF
-2) is a distinct clinical entity, characterized by multiple intracranial and spinal tumors.
While
bilateral
vestibular
schwannomas are the pathological hallmark of the
disease
, significant morbidity in
NF
-2 is attributable to the presence of both intramedullary and extramedullary spinal tumors.
With the advent of MRI as a screening modality, multiple, extensive spinal tumors in the
NF
-2 population are often seen, which may be clinically quiescent at the time of initial
diagnosis
.
All
NF
-2 patients should have routine screening with full spinal MRI at the time of
diagnosis
, regardless of symptoms.
[MeSH-major]
Neurofibromatosis 2
/
diagnosis
.
Neurofibromatosis 2
/ therapy. Spinal Neoplasms /
diagnosis
. Spinal Neoplasms / therapy
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(PMID = 19101145.001).
[ISSN]
0967-5868
[Journal-full-title]
Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
[ISO-abbreviation]
J Clin Neurosci
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Scotland
[Number-of-references]
44
78.
Hadfield KD, Newman WG, Bowers NL, Wallace A, Bolger C, Colley A, McCann E, Trump D, Prescott T, Evans DG:
Molecular characterisation of SMARCB1 and NF2 in familial and sporadic schwannomatosis.
J Med Genet
; 2008 Jun;45(6):332-9
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[Title]
Molecular characterisation of SMARCB1 and
NF2
in
familial
and sporadic schwannomatosis.
BACKGROUND: Schwannomatosis is a rare condition characterised by multiple schwannomas and lack of involvement of the
vestibular
nerve.
A recent report identified
bi
-allelic mutations in the SMARCB1/INI1 gene in a single family with schwannomatosis.
We aimed to establish the contribution of the SMARCB1 and the
NF2
genes to sporadic and
familial
schwannomatosis in our cohort.
METHODS: We performed DNA sequence and dosage analysis of SMARCB1 and
NF2
in 28 sporadic cases and 15 families with schwannomatosis.
In addition, in all affected individuals with SMARCB1 mutations and available tumour tissue, we detected
bi
-allelic somatic inactivation of the
NF2
gene.
CONCLUSION: In contrast to the recent report where no
NF2
mutations were identified in a schwannomatosis family with SMARCB1 mutations, in our cohort, a four hit model with mutations in both SMARCB1 and
NF2
define a subset of patients with schwannomatosis.
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[ErratumIn]
J Med Genet. 2008 Sep;45(9):608
(PMID = 18285426.001).
[ISSN]
1468-6244
[Journal-full-title]
Journal of medical genetics
[ISO-abbreviation]
J. Med. Genet.
[Language]
eng
[Grant]
United Kingdom / Cancer Research UK / / A6964; United Kingdom / Cancer Research UK / / C1389/A6964
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / Neurofibromin 2; 0 / SMARCB1 Protein; 0 / SMARCB1 protein, human; 0 / Transcription Factors
79.
Roser F, Ebner FH, Ritz R, Samii M, Tatagiba MS, Nakamura M:
Management of skull based meningiomas in the elderly patient.
J Clin Neurosci
; 2007 Mar;14(3):224-8
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BACKGROUND: The demographic evolution of Western society together with availability of modern imaging techniques leads to an increasing
diagnosis
of meningioma patients over 70 years of age.
DESIGN: Forty-three patients aged over 70 years were analyzed and matched in a retrospective study with a younger group of 89 patients according to tumour size, histology, symptoms, recurrence and presence of
neurofibromatosis II
.
[MeSH-minor]
Adult. Age Distribution. Aged. Aged, 80 and over. Humans. Middle Aged. Morbidity. Neoplasm Recurrence, Local / mortality.
Neurofibromatosis 2
/ mortality.
Neurofibromatosis 2
/ surgery. Patient Selection. Postoperative Complications / mortality. Quality of Life. Retrospective Studies
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(PMID = 17258130.001).
[ISSN]
0967-5868
[Journal-full-title]
Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
[ISO-abbreviation]
J Clin Neurosci
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Scotland
80.
Kobayashi H, Ishii N, Murata J, Saito H, Kubota KC, Nagashima K, Iwasaki Y:
Cystic meningioangiomatosis.
Pediatr Neurosurg
; 2006;42(5):320-4
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A 14-year-old boy without any stigmata of
neurofibromatosis type
2 presented intractable complex partial and generalized seizures since the age of 12 years.
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[Copyright]
Copyright 2006 S. Karger AG, Basel.
(PMID = 16902347.001).
[ISSN]
1016-2291
[Journal-full-title]
Pediatric neurosurgery
[ISO-abbreviation]
Pediatr Neurosurg
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
81.
Rice JM:
Inducible and transmissible genetic events and pediatric tumors of the nervous system.
J Radiat Res
; 2006;47 Suppl B:B1-11
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Tumors of the nervous system most often occur in both children and adults as sporadic events with no family history of the
disease
, but they are also among the clinical manifestations of a significant number of
familial
cancer syndromes, including
familial
retinoblastoma,
neurofibromatosis
1 and 2, tuberous sclerosis, and Cowden, Turcot, Li-Fraumeni and nevoid basal cell carcinoma (Gorlin) syndromes.
These genes include RB1, NF1,
NF2
, TSC1, TSC2, TP53, PTEN, APC, hMLH1, hPSM2, and PTCH, most of which function as tumor suppressor genes.
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(PMID = 17019046.001).
[ISSN]
1349-9157
[Journal-full-title]
Journal of radiation research
[ISO-abbreviation]
J. Radiat. Res.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / DNA, Neoplasm
[Number-of-references]
61
82.
Feucht M, Kluwe L, Mautner VF, Richard G:
Correlation of nonsense and frameshift mutations with severity of retinal abnormalities in neurofibromatosis 2.
Arch Ophthalmol
; 2008 Oct;126(10):1376-80
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[Title]
Correlation of nonsense and frameshift mutations with severity of retinal abnormalities in
neurofibromatosis 2
.
BACKGROUND:
Neurofibromatosis 2
(
NF2
) is an autosomal dominant
disease
that is characterized by nervous system tumors and ocular abnormalities.
OBJECTIVE: To investigate genotype-phenotype correlations demonstrated for
NF2
-associated nervous system tumors, cataracts, and retinal lesions.
METHODS: Forty-eight patients with
NF2
from a tertiary neurological referral center underwent screening for constitutional
NF2
mutations with multiple screening methods.
CONCLUSIONS: To our knowledge, this is the first genetic, clinical, and angiographic characterization of retinal abnormalities in
NF2
.
Clinical Relevance Retinal abnormalities, which can be revealed by means of fluorescein angiography, are more common in patients with
NF2
who have nonsense or frameshift mutations.
[MeSH-major]
Fluorescein Angiography. Frameshift Mutation. Genes,
Neurofibromatosis 2
.
Neurofibromatosis 2
/ epidemiology.
Neurofibromatosis 2
/ genetics. Retinal Diseases / epidemiology. Retinal Diseases / genetics
[MeSH-minor]
Adolescent. Adult. Age of Onset. Analysis of Variance. Cataract /
diagnosis
. Cataract / genetics. Causality. Child. Codon, Nonsense. Cohort Studies. Comorbidity. Confidence Intervals. Female. Genetic Predisposition to
Disease
. Genetic Testing. Genotype. Humans. Logistic Models. Male. Middle Aged. Odds Ratio. Phenotype. Severity of Illness Index
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(PMID = 18852415.001).
[ISSN]
1538-3601
[Journal-full-title]
Archives of ophthalmology (Chicago, Ill. : 1960)
[ISO-abbreviation]
Arch. Ophthalmol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Codon, Nonsense
83.
McLaughlin ME, Pepin SM, Maccollin M, Choopong P, Lessell S:
Ocular pathologic findings of neurofibromatosis type 2.
Arch Ophthalmol
; 2007 Mar;125(3):389-94
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[Title]
Ocular pathologic findings of
neurofibromatosis type
2.
OBJECTIVE: To gain insight into the pathogenesis of
neurofibromatosis type
2 (
NF2
) by investigating the ocular manifestations of this
disease
.
METHODS: Using standard histologic techniques, immunohistochemistry, and electron microscopy, we described the ocular pathologic findings of a 34-year-old woman who died from complications of
NF2
.
RESULTS: We identified 3 types of
NF2
-associated lesions: juvenile posterior subcapsular cataracts, epiretinal membranes, and an intrascleral
schwannoma
.
CONCLUSIONS: Our analysis indicated that dysplastic lens cells accumulate just anterior to the posterior lens capsule in juvenile posterior subcapsular cataracts and that dysplastic Müller cells may be a major component of
NF2
-associated epiretinal membranes.
Clinical Relevance Our findings suggest that a subset of glial cells with epithelial features (Schwann cells, ependymal cells, and Müller cells) may be particularly sensitive to loss of the
NF2
gene.
Understanding the molecular basis for this sensitivity may lead to novel strategies for treating
NF2
.
[MeSH-major]
Cataract / pathology. Epiretinal Membrane / pathology. Eye Neoplasms / pathology. Neurilemmoma / pathology.
Neurofibromatosis 2
/ pathology. Scleral Diseases / pathology
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.
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(PMID = 17353411.001).
[ISSN]
0003-9950
[Journal-full-title]
Archives of ophthalmology (Chicago, Ill. : 1960)
[ISO-abbreviation]
Arch. Ophthalmol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Glial Fibrillary Acidic Protein; 0 / Mucin-1; 0 / S100 Proteins; 68238-35-7 / Keratins
84.
Ahronowitz I, Xin W, Kiely R, Sims K, MacCollin M, Nunes FP:
Mutational spectrum of the NF2 gene: a meta-analysis of 12 years of research and diagnostic laboratory findings.
Hum Mutat
; 2007 Jan;28(1):1-12
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[Title]
Mutational spectrum of the
NF2
gene: a meta-analysis of 12 years of research and diagnostic laboratory findings.
The
NF2
tumor suppressor gene on chromosome 22 is a member of the protein 4.1 family of cytoskeletal elements.
A number of single- and multiple-tumor phenotypes have been linked to alterations of
NF2
since its characterization in 1993.
We present a meta-analysis of 967 constitutional and somatic
NF2
alterations from 93 published reports, along with 59 additional unpublished events identified in our laboratory and 115 alterations identified in clinical samples submitted to the Massachusetts General Hospital (MGH) Neurogenetics DNA Diagnostic Laboratory.
There was no statistically significant difference in mutation
type
or exon distribution between published constitutional events and those found by the clinical laboratory.
[MeSH-major]
Genes,
Neurofibromatosis 2
. Molecular Diagnostic Techniques / methods. Mutation
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[Copyright]
Published 2006 Wiley-Liss, Inc.
(PMID = 16983642.001).
[ISSN]
1098-1004
[Journal-full-title]
Human mutation
[ISO-abbreviation]
Hum. Mutat.
[Language]
eng
[Grant]
United States / NINDS NIH HHS / NS / 1 R01 NS40527
[Publication-type]
Journal Article; Meta-Analysis; Research Support, N.I.H., Extramural
[Publication-country]
United States
85.
Denayer E, Brems H, de Cock P, Evans GD, Van Calenbergh F, Bowers N, Sciot R, Debiec-Rychter M, Vermeesch JV, Fryns JP, Legius E:
Pathogenesis of vestibular schwannoma in ring chromosome 22.
BMC Med Genet
; 2009;10:97
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[Title]
Pathogenesis of
vestibular schwannoma
in ring chromosome 22.
Clinical features of
neurofibromatosis type
1 and 2 as well as different tumour types have been reported in patients with ring chromosome 22.
At the age of 20 years she was diagnosed with a unilateral
vestibular schwannoma
.
Tumour cells were analyzed by karyotyping, array CGH and
NF2
mutation analysis.
Genetic analysis of
vestibular schwannoma
tissue revealed loss of the ring chromosome 22 and a somatic second hit in the
NF2
gene on the remaining chromosome 22.
CONCLUSION: We conclude that tumours can arise by the combination of loss of the ring chromosome and a pathogenic
NF2
mutation on the remaining chromosome 22 in patients with ring chromosome 22.
Our findings indicate that patients with a ring 22 should be monitored for
NF2
-related tumours starting in adolescence.
[MeSH-major]
Chromosomes, Human, Pair 22.
Neuroma
,
Acoustic
/ genetics. Ring Chromosomes
[MeSH-minor]
Adult. Female. Genes,
Neurofibromatosis
1. Genes,
Neurofibromatosis 2
. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Magnetic Resonance Imaging. Mutation. Oligonucleotide Array Sequence Analysis. Phenotype. Sequence Analysis, DNA
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1471-2350
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BMC medical genetics
[ISO-abbreviation]
BMC Med. Genet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Other-IDs]
NLM/ PMC2758865
86.
Ye K:
Phosphorylation of merlin regulates its stability and tumor suppressive activity.
Cell Adh Migr
; 2007 Oct-Dec;1(4):196-8
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The
neurofibromatosis
-2 (
NF2
) tumor suppressor protein, merlin or schwannomin, inhibits cell proliferation by modulating the growth activities of its binding partners, including the cell surface glycoprotein CD44, membrane-cytoskeleton linker protein ezrin and PIKE (PI 3-kinase enhancer) GTPase, etc.
This
finding
demonstrates a negative feed-back loop from merlin/PIKE-L/PI 3-kinase to Akt in tumors- The proliferation repressive activity of merlin is also partially regulated by S518 phosphorylation- Thus, Akt-mediated merlin T230/S315 phosphorylation, combined with S518 phosphorylation by PAK and PKA, provides new insight into abrogating merlin function in the absence of merlin mutational inactivation.
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[ISSN]
1933-6926
[Journal-full-title]
Cell adhesion & migration
[ISO-abbreviation]
Cell Adh Migr
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA117872
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD44; 0 / CD44 protein, human; 0 / GTPase-Activating Proteins; 0 / Neurofibromin 2; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / p21-Activated Kinases; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.1.- / AGAP2 protein, human; EC 3.6.1.- / GTP-Binding Proteins
[Number-of-references]
21
[Other-IDs]
NLM/ PMC2634106
87.
Benesch M, Weber-Mzell D, Gerber NU, von Hoff K, Deinlein F, Krauss J, Warmuth-Metz M, Kortmann RD, Pietsch T, Driever PH, Quehenberger F, Urban C, Rutkowski S:
Ependymoma of the spinal cord in children and adolescents: a retrospective series from the HIT database.
J Neurosurg Pediatr
; 2010 Aug;6(2):137-44
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METHODS: Between 1991 and 2007, 29 patients (12 male and 17 female, median age at
diagnosis
13.6 years) with primary spinal cord ependymoma (myxopapillary ependymoma WHO Grade I,
II
, and III tumors in 6, 17, and 6 patients, respectively) were identified.
Four patients had
neurofibromatosis Type
2.
Seven patients (24.1%) developed progressive
disease
or relapse, 2 after gross-total resection (GTR) and 5 after incomplete resection or biopsy.
One patient with anaplastic ependymoma (WHO Grade III) died 65 months after
diagnosis
of
disease
progression.
[MeSH-minor]
Adolescent. Austria. Biopsy. Chemotherapy, Adjuvant. Child. Combined Modality Therapy. Disability Evaluation.
Disease
Progression. Female. Follow-Up Studies. Germany. Humans. Male.
Neurofibromatosis 2
/
diagnosis
.
Neurofibromatosis 2
/ drug therapy.
Neurofibromatosis 2
/ pathology.
Neurofibromatosis 2
/ radiotherapy.
Neurofibromatosis 2
/ surgery. Postoperative Complications /
diagnosis
. Postoperative Complications / mortality. Prospective Studies. Radiotherapy, Adjuvant. Registries. Survival Rate
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(PMID = 20672934.001).
[ISSN]
1933-0715
[Journal-full-title]
Journal of neurosurgery. Pediatrics
[ISO-abbreviation]
J Neurosurg Pediatr
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
United States
88.
Walcott BP, Sivarajan G, Bashinskaya B, Anderson DE, Leonetti JP, Origitano TC:
Sporadic unilateral vestibular schwannoma in the pediatric population. Clinical article.
J Neurosurg Pediatr
; 2009 Aug;4(2):125-9
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[Title]
Sporadic unilateral
vestibular schwannoma
in the pediatric population. Clinical article.
OBJECT:
Vestibular
schwannomas (VSs) are rare in the pediatric population.
Most often, these lesions manifest as a
bilateral
disease
process in the setting of
neurofibromatosis Type
2.
Clinical outcomes were reviewed with emphasis on facial nerve function and follow-up for signs and symptoms of a heritable
disorder
.
The average tumor size was 4.57 cm, with an average duration of symptoms prior to definitive
diagnosis
of 31.2 months.
At a follow-up average of 6.3 years (range 1-12 years), 100% of patients demonstrated good facial function (House-Brackmann Grade I or
II
).
No patient in this cohort demonstrated symptoms, objective signs, or genetic analysis indicating the presence of
neurofibromatosis Type
2.
CONCLUSIONS:
Diagnosis
and management of sporadic, unilateral VSs in children is complicated by clinical presentations and surgical challenges unique from their adult counterparts.
[MeSH-major]
Facial Nerve / physiopathology.
Neuroma
,
Acoustic
/ surgery
[MeSH-minor]
Adolescent. Child. Cohort Studies. Ear, Inner. Female. Humans. Male.
Neurofibromatosis 2
/ pathology. Recovery of Function. Retrospective Studies. Treatment Outcome
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(PMID = 19645545.001).
[ISSN]
1933-0707
[Journal-full-title]
Journal of neurosurgery. Pediatrics
[ISO-abbreviation]
J Neurosurg Pediatr
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
89.
Pitchford CW, Schwartz HS, Atkinson JB, Cates JM:
Soft tissue perineurioma in a patient with neurofibromatosis type 2: a tumor not previously associated with the NF2 syndrome.
Am J Surg Pathol
; 2006 Dec;30(12):1624-9
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[Title]
Soft tissue perineurioma in a patient with
neurofibromatosis type
2: a tumor not previously associated with the
NF2
syndrome.
Neoplasms that commonly affect patients with
neurofibromatosis type
2 (
NF2
) include schwannomas, meningiomas, astrocytomas, ependymomas, and neurofibromas.
As in both
NF2
-associated and sporadic cases of
schwannoma
and meningioma, perineuriomas often harbor mutations or deletions of the
NF2
gene.
However, perineuriomas have not previously been reported in the clinical setting of
NF2
.
A 30-year-old man with a history of
bilateral
vestibular
schwannomas, a parasagittal meningioma, an intraspinal ependymoma, and multiple other neoplasms involving both cranial and peripheral nerves (thereby fulfilling the diagnostic criteria for
NF2
) presented with an enlarging thigh mass.
The
diagnosis
of cellular soft tissue perineurioma was confirmed by both immunohistochemical and ultrastructural analysis.
This case represents the first report of a soft tissue perineurioma arising in the setting of
NF2
.
[MeSH-major]
Nerve Sheath Neoplasms / complications.
Neurofibromatosis 2
/ complications. Soft Tissue Neoplasms / complications
[MeSH-minor]
Adult. Biomarkers, Tumor / analysis. Cytoplasm / ultrastructure.
Diagnosis
, Differential. Humans. Male. Neoplasms, Multiple Primary. Peripheral Nervous System Neoplasms /
diagnosis
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(PMID = 17122521.001).
[ISSN]
0147-5185
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor
90.
Skarzynski H, Lorens A, Kochanek K, Mrowka M, Behr R:
Bilateral auditory brainstem implantation in a patient with neurofibromatosis type II.
Cochlear Implants Int
; 2010 Jun;11 Suppl 1:88-93
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[Title]
Bilateral
auditory brainstem implantation in a patient with
neurofibromatosis type II
.
[MeSH-major]
Auditory Brain Stem Implantation / methods.
Neurofibromatosis 2
/ surgery.
Neuroma
,
Acoustic
/ surgery. Neurosurgical Procedures / methods
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(PMID = 21756589.001).
[ISSN]
1754-7628
[Journal-full-title]
Cochlear implants international
[ISO-abbreviation]
Cochlear Implants Int
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
91.
Slattery WH 3rd, Fisher LM, Hitselberger W, Friedman RA, Brackmann DE:
Hearing preservation surgery for neurofibromatosis Type 2-related vestibular schwannoma in pediatric patients.
J Neurosurg
; 2007 Apr;106(4 Suppl):255-60
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[Title]
Hearing preservation surgery for
neurofibromatosis Type
2-related
vestibular schwannoma
in pediatric patients.
OBJECT: The authors reviewed the proportion of pediatric patients with
neurofibromatosis Type
2 (
NF2
) in whom hearing was preserved after middle fossa resection of
vestibular schwannoma
(VS).
METHODS: In this retrospective chart review the authors examined the cases of 35 children with
NF2
who had undergone middle fossa resection (47 surgeries) between 1992 and 2004 in a neurotological tertiary care center.
Facial nerve function was good (House-Brackmann Grades I or
II
) in 81% of the patients.
Twelve patients had
bilateral
middle fossa resections; in nine (75%) of these patients hearing was maintained postoperatively in both ears.
CONCLUSIONS: More than half of the children with
NF2
in the authors' cohort experienced hearing preservation after middle fossa resection was performed for vs. The authors recommend this approach for preserving hearing in children with
NF2
.
[MeSH-major]
Facial Nerve / physiopathology. Hearing / physiology.
Neurofibromatosis 2
/ surgery.
Neuroma
,
Acoustic
/ surgery
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.
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(PMID = 17465357.001).
[ISSN]
0022-3085
[Journal-full-title]
Journal of neurosurgery
[ISO-abbreviation]
J. Neurosurg.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
92.
Scoles DR, Yong WH, Qin Y, Wawrowsky K, Pulst SM:
Schwannomin inhibits tumorigenesis through direct interaction with the eukaryotic initiation factor subunit c (eIF3c).
Hum Mol Genet
; 2006 Apr 1;15(7):1059-70
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The
neurofibromatosis 2
(
NF2
) tumor suppressor protein, schwannomin or merlin, is commonly lost upon
NF2
gene mutation in benign human brain tumors.
Consequently, eIF3c appears to be involved in
NF2
pathogenesis and deserves to be investigated as a prognostic marker for
NF2
and target for treatment of
NF2
patient tumors.
[MeSH-minor]
Adult. Cell Line, Transformed. Cell Proliferation. Fluorescent Antibody Technique. Gene Expression Regulation, Neoplastic. Humans. Immunoprecipitation. Meningioma / metabolism. Meningioma / pathology. Models, Biological.
Neurofibromatoses
/ metabolism. Protein Structure, Tertiary. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Tumor Cells, Cultured
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(PMID = 16497727.001).
[ISSN]
0964-6906
[Journal-full-title]
Human molecular genetics
[ISO-abbreviation]
Hum. Mol. Genet.
[Language]
eng
[Grant]
United States / NINDS NIH HHS / NS / KO8NS001428; United States / NINDS NIH HHS / NS / R01NS037883
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Eukaryotic Initiation Factor-3; 0 / Neurofibromin 2; 0 / Recombinant Proteins
93.
Chan AW, Black P, Ojemann RG, Barker FG 2nd, Kooy HM, Lopes VV, McKenna MJ, Shrieve DC, Martuza RL, Loeffler JS:
Stereotactic radiotherapy for vestibular schwannomas: favorable outcome with minimal toxicity.
Neurosurgery
; 2005 Jul;57(1):60-70; discussion 60-70
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[Title]
Stereotactic radiotherapy for
vestibular
schwannomas: favorable outcome with minimal toxicity.
OBJECTIVE: To determine the outcome and toxicity in patients with
vestibular
schwannomas treated with conventionally fractionated stereotactic radiotherapy (SRT) and to identify prognostic factors that are predictive of outcome.
METHODS: Between 1992 and 2001, 70 patients with
vestibular
schwannomas were treated with linear accelerator-based SRT in our institutions.
Eleven patients had
neurofibromatosis Type II
(
NF2
).
There was no difference in tumor control and cranial nerve function preservation rates seen in
NF2
patients compared with non-
NF2
patients.
[MeSH-major]
Dose Fractionation.
Neuroma
,
Acoustic
/ surgery. Radiosurgery / methods. Stereotaxic Techniques. Treatment Outcome
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(PMID = 15987541.001).
[ISSN]
1524-4040
[Journal-full-title]
Neurosurgery
[ISO-abbreviation]
Neurosurgery
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article
[Publication-country]
United States
94.
An JH, Seong J, Oh H, Kim W, Han KH, Paik YH:
[Protein expression profiles in a rat cirrhotic model induced by thioacetamide].
Korean J Hepatol
; 2006 Mar;12(1):93-102
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BACKGROUND/AIMS: The reactive oxygen species from thioacetamide (TAA) induces rat liver cirrhosis that resembles the human
disease
, and it can serve as a suitable animal model for studying human liver cirrhosis.
In contrast, the expression level of the proteins did not show a significant change at 9 weeks, but this increased to 3-fold at 30 weeks for carbonic anhydrase VII, ras related protein Rab 6, Annexin A2,
neurofibromatosis type
2 and aldehyde dehydrogenase.
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(PMID = 16565610.001).
[ISSN]
1738-222X
[Journal-full-title]
The Korean journal of hepatology
[ISO-abbreviation]
Korean J Hepatol
[Language]
kor
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Proteins; 075T165X8M / Thioacetamide
95.
Beyer KS, Beauchamp RL, Lee MF, Gusella JF, Näär AM, Ramesh V:
Mediator subunit MED28 (Magicin) is a repressor of smooth muscle cell differentiation.
J Biol Chem
; 2007 Nov 2;282(44):32152-7
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Magicin, a protein that we isolated earlier as an interactor of the
neurofibromatosis 2
protein merlin, was independently identified as MED28, a subunit of the mammalian Mediator complex.
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(PMID = 17848560.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Grant]
United States / NINDS NIH HHS / NS / NS24279; United States / NINDS NIH HHS / NS / NS45776
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Cytoskeletal Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / MED28 protein, human; 0 / Mediator Complex
96.
Xiao GH, Gallagher R, Shetler J, Skele K, Altomare DA, Pestell RG, Jhanwar S, Testa JR:
The NF2 tumor suppressor gene product, merlin, inhibits cell proliferation and cell cycle progression by repressing cyclin D1 expression.
Mol Cell Biol
; 2005 Mar;25(6):2384-94
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[Title]
The
NF2
tumor suppressor gene product, merlin, inhibits cell proliferation and cell cycle progression by repressing cyclin D1 expression.
Inactivation of the
NF2
tumor suppressor gene has been observed in certain benign and malignant tumors.
Recent studies have demonstrated that merlin, the product of the
NF2
gene, is regulated by Rac/PAK signaling.
In this report, we show that adenovirus-mediated expression of merlin in
NF2
-deficient tumor cells inhibits cell proliferation and arrests cells at G1 phase, concomitant with decreased expression of cyclin D1, inhibition of CDK4 activity, and dephosphorylation of pRB.
RNA interference experiments showed that silencing of the endogenous
NF2
gene results in upregulation of cyclin D1 and S-phase entry.
Furthermore, PAK1-stimulated cyclin D1 promoter activity was repressed by cotransfection of
NF2
, and PAK activity was inhibited by expression of merlin.
Interestingly, the S518A mutant form of merlin, which is refractory to phosphorylation by PAK, was more efficient than the wild-
type
protein in inhibiting cell cycle progression and in repressing cyclin D1 promoter activity.
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[ISSN]
0270-7306
[Journal-full-title]
Molecular and cellular biology
[ISO-abbreviation]
Mol. Cell. Biol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA075503; United States / NCI NIH HHS / CA / R01 CA093596; United States / NCI NIH HHS / CA / R01 CA045745; United States / NCI NIH HHS / CA / R29 CA070896; United States / NCI NIH HHS / CA / R01 CA070896; United States / PHS HHS / / T32-16850; United States / NCI NIH HHS / CA / CA-45745; United States / NCI NIH HHS / CA / CA-75503; United States / NCI NIH HHS / CA / CA-93596; United States / NCI NIH HHS / CA / R01 CA086072; United States / NCI NIH HHS / CA / CA-86072; United States / NCI NIH HHS / CA / P30 CA006927; United States / NCI NIH HHS / CA / CA-70896; United States / NCI NIH HHS / CA / CA-06927
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Neurofibromin 2; 0 / RNA, Small Interfering; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / PAK1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / p21-Activated Kinases
[Other-IDs]
NLM/ PMC1061616
97.
Ikeda T, Hashimoto S, Fukushige S, Ohmori H, Horii A:
Comparative genomic hybridization and mutation analyses of sporadic schwannomas.
J Neurooncol
; 2005 May;72(3):225-30
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Schwannomas of the
vestibular
nerve are the striking characteristics of
neurofibromatosis type
2 (
NF2
), an autosomal dominant hereditary
disease
.
The
NF2
gene on 22q12 has been isolated as the gene responsible for
NF2
.
Previous studies have reported that 60% of sporadic schwannomas showed inactivation of the
NF2
gene, but genetic alterations of remaining 40% tumors remain elusive.
Loss of chromosome 22q, including the
NF2
locus, was the only notable abnormality (5/17, 29%).
Further, we performed fluorescence in situ hybridization analysis with a genomic BAC clone harboring the
NF2
gene and found that the 5 tumors with loss detected by CGH as well as three cases without such a detectable loss by CGH, or a total, 8/17 (47%), showed loss of the
NF2
locus.
Mutation search by PCR-SSCP followed by direct sequencing revealed that 71% (12/17) of the tumors had one or two mutations in the
NF2
gene.
Our analyses disclosed that 14 (82%) of 17 tumors had structural alteration of
NF2
; among these 14 cases, 9 (64%) had two inactivating mutations in the
NF2
gene, either a somatic mutation in one allele coupled with loss of the other allele or two independent somatic mutations.
Our present results suggested that (i) most of the sporadic schwannomas have two-hit mutations in the
NF2
gene, and (
ii
)
NF2
is the only major causative gene in the genesis of schwannomas that is activated or inactivated by copy number alterations.
[MeSH-minor]
Adult. Aged. DNA Mutational Analysis. DNA Primers. Female. Genes,
Neurofibromatosis 2
. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Nucleic Acid Hybridization. Polymorphism, Single-Stranded Conformational. Reverse Transcriptase Polymerase Chain Reaction
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