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Reversible tumorigenesis by MYC in hematopoietic lineages

D W Felsher1, J M Bishop

  • 1Department of Medicine, G. W. Hooper Foundation, San Francisco, California, USA. felsher@itsa.ucsf.edu

Molecular Cell
|September 17, 1999
PubMed

Insights

Targeting the MYC protooncogene in hematopoietic cells can effectively treat cancer. Inactivating MYC in mice with lymphoma or leukemia caused tumor regression, demonstrating the potential of single genetic lesion remediation for cancer therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Targeted therapies offer potential for treating human neoplasia by addressing specific genetic mutations.
  • Protooncogenes, like MYC, play critical roles in cell growth and can drive cancer development when dysregulated.

Purpose of the Study:

  • To investigate the therapeutic potential of conditionally inactivating the MYC protooncogene in hematopoietic cells.
  • To determine if targeting a single genetic lesion can reverse established malignancy.

Main Methods:

  • Generation of transgenic mice using the tetracycline regulatory system for conditional MYC protooncogene expression in hematopoietic cells.
  • Induction of tumors (T cell lymphomas, acute myeloid leukemias) via sustained MYC expression.
  • Inactivation of the MYC transgene to observe tumor response.

Main Results:

  • Sustained MYC expression led to the development of malignant T cell lymphomas and acute myeloid leukemias.
  • Inactivation of the MYC transgene resulted in the regression of established tumors.
  • Tumor regression was characterized by proliferative arrest, differentiation, apoptosis, and restoration of normal hematopoiesis.

Conclusions:

  • Conditional inactivation of the MYC protooncogene can effectively reverse established hematopoietic malignancies in a mouse model.
  • Remediation of a single genetic lesion, even in a multistep process like tumorigenesis, can be sufficient to reverse malignancy.
  • This study supports the development of targeted therapies for cancer based on specific genetic alterations.

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