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Genomic imprinting and carcinogenesis

K Yun1

  • 1Cancer Research Laboratory, Department of Pathology, Dunedin School of Medicine, University of Otago, New Zealand.

Histology and Histopathology
|May 20, 1998
PubMed
Summary
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Genomic imprinting, where parental origin affects gene expression, deviates from Mendelian inheritance. Loss of imprinting (LOI) in genes like IGF2 is linked to Wilms tumor and other cancers.

Area of Science:

  • Genetics
  • Developmental Biology
  • Epigenetics

Background:

  • Mendelian inheritance typically involves equal expression from parental alleles.
  • Genomic imprinting is an exception where allele expression depends on parental origin.
  • This phenomenon has implications for genetics, evolution, development, and pathology.

Purpose of the Study:

  • To review genomic imprinting, focusing on the Insulin-like Growth Factor 2 (IGF2) gene.
  • To discuss the role of IGF2 imprinting and loss of imprinting (LOI) in Wilms tumor (WT) and other cancers.
  • To explore other imprinted genes on chromosome 11p15 and the molecular mechanisms of imprinting.

Main Methods:

  • Literature review of genomic imprinting.
  • Focus on IGF2 gene imprinting and its association with cancer.

Related Experiment Videos

  • Discussion of molecular mechanisms and related imprinted genes.

    • Main Results:

    • IGF2 is imprinted, with paternal expression and maternal silencing, conserved across species.
    • Loss of imprinting (LOI) of IGF2 is observed in numerous tumor types, including Wilms tumor.
    • LOI of IGF2 may lead to deregulated expression, potentially initiating tumor development.

    Conclusions:

    • Genomic imprinting is a significant epigenetic mechanism with broad biological relevance.
    • Loss of imprinting in IGF2 is implicated in Wilms tumor pathogenesis and potentially other cancers.
    • Further research into imprinted genes and their mechanisms is crucial for understanding disease development.