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a Division of
Pediatric Hematology and Oncology, The Ohio State University and the
Comprehensive Cancer Center, Columbus, Ohio 43210, USA, b Division
of Human Cancer Genetics, The Ohio State University and the
Comprehensive Cancer Center, Columbus, Ohio 43210, USA, c Department of
Neuroscience, The Ohio State University and the Comprehensive Cancer
Center, Columbus, Ohio 43210, USA, d Department
of Veterinary Biosciences, The Ohio State University and the
Comprehensive Cancer Center, Columbus, Ohio 43210, USA, e Department of Biochemistry and Molecular
Biology, Mayo Clinic, Rochester, Minnesota 55905, USA, f Department of Pathology, The Ohio
State University and the Comprehensive Cancer Center, Columbus, Ohio
43210, USA, g University of
California, San Francisco, CA 94115-0128, USA, h Division of Oncology, The Children's
Hospital of Philadelphia and the University of Pennsylvania,
Philadelphia, Pennsylvania 19104-4318, USA
Correspondence to: Dr Frühwald, Westfälische Wilhelms-Universität Münster, Klinik und Poliklinik für Kinderheilkunde, Pädiatrische Hämatologie/Onkologie, Albert-Schweizer-Strasse 33, 48149 Münster, Germany, fruhwald{at}uni-muenster.de or Dr Plass, plass-1{at}medctr.osu.edu
Revised version received 14 February
2000;
Accepted for publication 18 February 2000
OBJECTIVES
The pathological entity
of primitive neuroectodermal tumour/medulloblastoma (PNET/MB) comprises
a very heterogeneous group of neoplasms on a clinical as well as on a
molecular level. We evaluated the importance of DNA amplification in
medulloblastomas and other primitive neuroectodermal tumours (PNETs) of
the CNS.
METHODRestriction landmark genomic
scanning (RLGS), a method that allows the detection of low level
amplification, was used. RLGS provides direct access to DNA sequences
circumventing positional cloning efforts. Furthermore, we analysed
several samples by CGH.
DESIGNTwenty primary
medulloblastomas, five supratentorial PNETs, and five medulloblastoma
cell lines were studied.
RESULTSAlthough our analysis
confirms that gene amplification is generally a rare event in childhood
PNET/MB, we found a total of 17 DNA fragments that were amplified in
seven different tumours. Cloning and sequencing of several of these
fragments confirmed the previous finding of
MYC amplification in the cell line D341 Med
and identified novel DNA sequences amplified in PNET/MB. We describe
for the first time amplification of the novel gene,
NAG, in a subset of PNET/MB. Despite genomic
amplification, NAG was not overexpressed in
the tumours studied. We have determined that NAG maps less than 50 kb 5' of
DDX1 and approximately 400 kb telomeric of
MYCN on chromosome 2p24.
CONCLUSIONWe found a similar but
slightly higher frequency of amplification than previously reported. We
present several DNA fragments that may belong to the CpG islands of
novel genes amplified in a small subset of PNET/MB. As an example we
describe for the first time the amplification of
NAG in the MYCN
amplicon in PNET/MB.
This article has been cited by other articles:
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 Z. Dai, W.-G. Zhu, C. D. Morrison, R. M. Brena, D. J. Smiraglia, A. Raval, Y.-Z. Wu, L. J. Rush, P. Ross, J. R. Molina, et al. A comprehensive search for DNA amplification in lung cancer identifies inhibitors of apoptosis cIAP1 and cIAP2 as candidate oncogenes Hum. Mol. Genet., April 1, 2003; 12(7): 791 - 801. [Abstract] [Full Text] [PDF]
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 Z. Dai, D. Weichenhan, Y.-Z. Wu, J. L Hall, L. J. Rush, L. T. Smith, A. Raval, L. Yu, D. Kroll, J. Muehlisch, et al. An AscI Boundary Library for the Studies of Genetic and Epigenetic Alterations in CpG Islands Genome Res., October 1, 2002; 12(10): 1591 - 1598. [Abstract] [Full Text] [PDF]
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 J. F Costello and C. Plass Methylation matters J. Med. Genet., May 1, 2001; 38(5): 285 - 303. [Abstract] [Full Text]
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