跪求论文翻译，不要在线翻译，谢谢!!!

Introduction
About 25% to 30% of primary untreated neuroblastomas
present amplification/overexpression of the MYCN protooncogene,
which is associated with advanced stage disease,
rapid progression, and poor prognosis (1).
Targeted expression of MYCN in transgenic mice causes
development of neuroblastoma (2). Unlike MYC, which is
fairly ubiquitous and is expressed in proliferating cells,
MYCN has a very restricted expression pattern (in mice,
MYCN is mainly expressed during the early stages of
differentiation, and in early B-cell development in adults;
ref. 3). Identification of selective inhibitors of N-Myc could
be relevant for development of more effective and less toxic
specific therapeutic agents for neuroblastomas with MYCN
overexpression. Antisense oligodeoxynucleotide–based
inhibition of MYCN expression in vitro decreases neuroblastoma
proliferation and promotes neuron differentiation
(4). A maj

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