Publication: Genomic imprinting and carcinogenesis
Authors
Yun, K.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The Mendelian inheritance is based on the
fundamental rule in which mammalian genes are
expressed equally from two homologous biparental
alleles. Recently a small number of genes have been
identified to show an exception to this rule in that
homologous alleles can function differently in somatic
cells depending on whether they come from the mother
or the father. This intriguing biological phenomenon is
called as genomic imprinting which does not conform
classical Mendelian inheritance and has potentially far
reaching implications for genetics, evolution,
developmental biology and pathology including cancer.
The gene encoding insulin-like growth factor 2 (IGF2)
harbors at llp15.5 and serves as paradigm for an
imprinted gene. The lGF2 gene has been demonstrated
to be imprinted with the paternal allele expressed and the
maternal being silent which is evolutionally conserved
between mice and human. Loss of imprinting (L01) of
IGF2 has been demonstrated in a dozen of tumor types
including Wilms tumor (WT) with a promise of many
more to come. The LOT of IGF2 may induce increased
or dcrcgulated IGF2 expression which could initiate the
onset of WT. Thus the L01 of IGF2 may provide a novel
mechanism of gene activation and play a role in the
development of a wide range of tumors. This review also
discusses other imprinted genes on llp15 which may
have a role in WT or other diseases. Finally molecular
mechanisms of genomic imprinting are discussed.
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