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MYC Inactivation Elicits Oncogene Addiction through Both Tumor Cell-Intrinsic and Host-Dependent Mechanisms

Dean W Felsher1

  • 1Division of Oncology, Departments of Medicine and Pathology, Stanford University, Stanford, CA, USA.

Genes & Cancer
|November 2, 2010
PubMed

Insights

Inactivating the MYC oncogene shows promise as a cancer therapy. This approach leverages oncogene addiction to induce tumor regression across various cancer types.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Tumorigenesis often involves genetic alterations activating oncogenes or deactivating tumor suppressor genes.
  • Oncogene addiction describes tumor regression following targeted inactivation of activated oncogenes.
  • MYC oncogene activation is a frequent event in human cancers.

Purpose of the Study:

  • To investigate the therapeutic potential of MYC oncogene inactivation in cancer treatment.
  • To explore the mechanisms underlying tumor regression induced by MYC inactivation.

Main Methods:

  • Experimental inactivation of the MYC oncogene in various cancer models.
  • Analysis of tumor regression and associated cellular and molecular changes.
  • Investigation of cell-autonomous and cell-dependent mechanisms, including autocrine factors.

Main Results:

  • MYC inactivation led to significant and sustained tumor regression in multiple cancer types (lymphoma, leukemia, osteosarcoma, etc.).
  • Mechanisms of regression include proliferative arrest, differentiation, senescence, apoptosis, and anti-angiogenesis.
  • Both cell-intrinsic and host-dependent pathways, involving factors like thrombospondin-1 and TGF-β, contribute to tumor regression.

Conclusions:

  • Targeting MYC inactivation represents a potential broad-spectrum cancer therapy.
  • This strategy exploits oncogene addiction, leading to tumor regression via diverse mechanisms.
  • Both tumor cell-autonomous and host-mediated responses are crucial for therapeutic efficacy.
Keywords:
MYConcogene addictiontumorigenesis

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