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A developmental context for multiple genetic alterations in Wilms' tumor

A P Feinberg1

  • 1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.

Journal of Cell Science. Supplement
|January 1, 1994
PubMed
Summary

Wilms

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Area of Science:

  • Oncology
  • Genetics
  • Developmental Biology

Background:

  • Wilms' tumor genetics is complex, challenging the initial two-hit hypothesis.
  • The Wilms' tumor 1 (WT1) gene on 11p13 is mutated in a minority of cases.
  • A second Wilms' tumor gene on 11p15 and genomic imprinting are also implicated.

Purpose of the Study:

  • To propose a comprehensive model for Wilms' tumorigenesis.
  • To account for the heterogeneity observed in Wilms' tumor epidemiology and pathology.
  • To explain the tissue-specific nature of tumors arising from these genetic alterations.

Main Methods:

  • Review and synthesis of existing genetic and epidemiological data on Wilms' tumor.
  • Analysis of the roles of specific genes (WT1) and chromosomal regions (11p13, 11p15).
  • Consideration of epigenetic factors like genomic imprinting.

Main Results:

  • Wilms' tumor arises from multiple genetic alterations, not solely WT1 mutations.
  • Genomic imprinting disruptions are early events in tumorigenesis.
  • Genes on other chromosomes contribute to tumor development.
  • A complex interplay of genetic and epigenetic factors within a developmental context is crucial.

Conclusions:

  • Wilms' tumorigenesis is a multi-step process involving multiple genetic and epigenetic alterations.
  • A proposed model integrates these factors to explain tumor heterogeneity and tissue specificity.
  • Understanding this complexity is key to further research in Wilms' tumor and other cancers.

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