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Oncogenesis

A twist in the tale

Nature Reviews Cancer volume 2, page 560 (2002)Cite this article

Inactivating oncogenes would seem to be a sensible approach for treating cancer, but the toxicity that is associated with this can be high because most oncogenes are also essential for the growth of normal cells. Inactivating oncogenes for just a short period of time could solve the toxicity problem, but would tumours regrow following oncogene reactivation? The authors investigated this question by expressing c-MYC in mice lymphocytes behind the regulatable tetracycline promoter.

This mouse model has recently been shown to induce osteogenic sarcomas — apparently c-MYC is also expressed in immature osteoblasts — which share features with human osteogenic sarcomas, such as frequent metastasis. Switching off c-MYC by administering doxycycline caused the tumours to regress and the cells to differentiate into bone.

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References

ORIGINAL RESEARCH PAPER

  1. Jain, M. et al. Sustained loss of neoplastic phenotype by inactivation of MYC. Science 297, 102–104 (2002)

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FURTHER READING

  1. Weinstein, I. B. Addiction to oncogenes — the achilles heal of cancer. Science 297, 63–64 (2002)

    Article  CAS  Google Scholar 

  2. Felsher, D. W. & Bishop, J. M. Reversible tumorigenesis by MYC in hematopoietic lineages. Mol. Cell 4, 199–207 (1999)

    Article  CAS  Google Scholar 

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Authors
  1. Emma Greenwood
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Greenwood, E. A twist in the tale. Nat Rev Cancer 2, 560 (2002). https://doi.org/10.1038/nrc868

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  • DOI: https://doi.org/10.1038/nrc868

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