Journal of the National Cancer Institute Advance Access originally published
online on February 12, 2008
JNCI Journal of the National Cancer Institute 2008 100(4):270-276;
doi:10.1093/jnci/djn004








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© The Author 2008. Published by Oxford University Press.









ARTICLES






Comprehensive Analysis of DNA Repair Gene Variants and Risk of Meningioma
Lara Bethke, Anne Murray, Emily Webb, Minouk Schoemaker, Kenneth Muir, Patricia
McKinney, Sarah Hepworth, Polyxeni Dimitropoulou, Artitaya Lophatananon, Maria
Feychting, Stefan Lönn, Anders Ahlbom, Beatrice Malmer, Roger Henriksson, Anssi
Auvinen, Anne Kiuru, Tiina Salminen, Christoffer Johansen, Helle Collatz
Christensen, Michael Kosteljanetz, Anthony Swerdlow, Richard Houlston
Affiliations of authors: Sections of Cancer Genetics (LB, AM, EW, RH) and
Epidemiology (MS, AS), Institute of Cancer Research, Sutton, UK; Division of
Epidemiology and Public Health, University of Nottingham Medical School
Queen’s Medical Centre, Nottingham, UK (KM, PD, AL); Centre for Epidemiology
and Biostatistics, University of Leeds, UK (PM, SH); Division of Epidemiology,
Institute of Environmental Medicine (MF, A. Ahlbom) and Department of Medical
Epidemiology and Biostatistics (SL), Karolinska Institutet, Stockholm, Sweden;
Department of Radiation Sciences, Oncology, Umeå University, Sweden (BM, RH);
Department of Epidemiology, Tampere School of Public Health, University of
Tampere, Finland (A. Auvinen, TS); Department of Research and Environmental
Surveillance, Radiation and Nuclear Safety Authority, STUK, Helsinki, Finland
(A. Auvinen, AK, TS); Institute of Cancer Epidemiology, Danish Cancer Society,
Copenhagen, Denmark (CJ, HCC); Neurosurgical Department, Rigshospitalet,
Copenhagen, Denmark (MK)

Correspondence to: Richard Houlston, PhD, Section of Cancer Genetics, Institute
of Cancer Research, 15 Cotswold Rd, Sutton, Surrey SM2 5NG, UK (e-mail:
richard.houlston@... ).

Background: Meningiomas account for up to 37% of all primary brain tumors.
Genetic susceptibility to meningioma is well established, with the risk among
relatives of meningioma patients being approximately threefold higher than that
in the general population. A relationship between risk of meningioma and
exposure to ionizing radiation is also well known and led us to examine whether
variants in DNA repair genes contribute to disease susceptibility.

Methods: We analyzed 1127 tagging single-nucleotide polymorphisms (SNPs) that
were selected to capture most of the common variation in 136 DNA repair genes in
five case–control series (631 case patients and 637 control subjects) from
four countries in Europe. We also analyzed 388 putative functional SNPs in these
genes for their association with meningioma. All statistical tests were
two-sided.

Results: The SNP rs4968451, which maps to intron 4 of the gene that encodes
breast cancer susceptibility gene 1–interacting protein 1, was consistently
associated with an increased risk of developing meningioma. Across the five
studies, the association was highly statistically significant (trend odds ratio
= 1.57, 95% confidence interval = 1.28 to 1.93; Ptrend = 8.95 x 10–6; P = .009
after adjusting for multiple testing).

Conclusions: We have identified a novel association between rs4968451 and
meningioma risk. Because approximately 28% of the European population are
carriers of at-risk genotypes for rs4968451, the variant is likely to make a
substantial contribution to the development of meningioma.







CONTEXT AND CAVEATS
Prior knowledge

Meningioma is an uncommon tumor that occurs in the brain, and relatives of
meningioma patients have an increased risk of developing the disease. Risk of
meningioma is also associated with exposure to ionizing radiation.

Study design

Analysis of single-nucleotide polymorphisms (SNPs) in DNA repair genes and their
associations with meningioma risk in populations from five case–control
studies in northern Europe.

Contribution

A SNP that is located in the coding portion of the gene for the breast cancer
susceptibility gene 1–interacting protein 1 was associated with increased risk
for meningioma.

Implication

The SNP identified may contribute substantially to meningioma risk because
almost 30% of the European population carry the genetic variation.

Limitations

The study was performed using participants from four countries in Europe who
were chosen based on their ethnicity, so how these results may apply to other
populations is still unclear. The functional consequence of the genetic
variation and how it may contribute to the development of meningioma are
unknown.






 
Manuscript received August 30, 2007; revised December 7, 2007; accepted January
7, 2008.








-----Original Message-----
From: Cindirixey@...
To: meningioma@...
Sent: Mon, 31 Mar 2008 2:14 pm
Subject: [MNG] recent research radiosurgery results



http://www.brainlife.org/newsletter/2008/v07n06.htm

 

http://www.neurosurgery-online.com/pt/re/neurosurg/abstract.00006123-200801000-0\
0004.htm;jsessionid=HxTDkthQvzLS1wLVlVS6rsthvznv8RBGyDJKKJN6JNh9WVygw0Dh!1569501\
743!181195629!8091!-1

 

 







January 2008, 62:1 > RADIOSURGERY AS DEFINITIVE MANAGEMENT...



 






ARTICLE LINKS:
Fulltext  |  PDF (979 K)


RADIOSURGERY AS DEFINITIVE MANAGEMENT OF INTRACRANIAL MENINGIOMAS.

CLINICAL STUDIES
Neurosurgery. 62(1):53-60, January 2008.
Kondziolka, Douglas M.D., M.Sc.; Mathieu, David M.D.; Lunsford, L. Dade M.D.;
Martin, Juan J. M.D.; Madhok, Ricky M.D.; Niranjan, Ajay M.Ch.; Flickinger, John
C. M.D.

Abstract:
OBJECTIVE: Stereotactic radiosurgery has become an important primary or adjuvant
minimally invasive management strategy for patients with intracranial
meningiomas with the goals of long-term tumor growth prevention and maintenance
of patient neurological function. We evaluated clinical and imaging outcomes of
meningiomas stratified by histological tumor grade.

METHODS: The patient cohort consisted of 972 patients with 1045 intracranial
meningiomas managed during an 18-year period. The series included 70% women, 49%
of whom had undergone a previous resection and 5% of whom had received previous
fractionated radiation therapy. Tumor locations included middle fossa (n = 351),
posterior fossa (n = 307), convexity (n = 126), anterior fossa (n = 88),
parasagittal region (n = 113), or other (n = 115).

RESULTS: The overall control rate for patients with benign meningiomas (World
Health Organization Grade I) was 93%. In those without previous histological
confirmation (n = 482), tumor control was 97%. However, for patients with World
Health Organization Grade II and III tumors, tumor control was 50 and 17%,
respectively. Delayed resection after radiosurgery was necessary in 51 patients
(5%) at a mean of 35 months. After 10 years, Grade 1 tumors were controlled in
91% (n = 53); in those without histology, 95% (n = 22) were controlled. None of
the patients developed a radiation-induced tumor. The overall morbidity rate was
7.7%. Symptomatic peritumoral imaging changes developed in 4% of the patients at
a mean of 8 months.

CONCLUSION: Stereotactic radiosurgery provided high rates of tumor growth
control or regression in patients with benign meningiomas with low risk. This
study confirms the role of radiosurgery as an effective management choice for
patients with small to medium-sized symptomatic, newly diagnosed or recurrent
meningiomas of the brain.

Copyright (C) by the Congress of Neurological Surgeons








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