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c-Myc and activated Ras during skin tumorigenesis: cooperation at the cancer stem cell level?

A Trumpp1

  • 1Genetics and Stem Cell Laboratory, Swiss Institute for Experimental Cancer Research (ISREC), Ch. des Boveresses 155, CH-1066 Epalinges, Switzerland. Andreas.Trumpp@isrec.ch

Ernst Schering Foundation Symposium Proceedings
|October 18, 2007
PubMed

Insights

Oncogenes Myc and Ras drive cancer by cooperating to overcome cell death signals. This review explores c-Myc

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Myc and Ras oncogene activation are frequent in cancers.
  • They exemplify oncogene cooperation, where their individual tumor-suppressive effects (apoptosis for Myc, senescence for Ras) are mutually antagonized.
  • Understanding this interplay is crucial for cancer therapy.

Purpose of the Study:

  • To review the role of endogenous and overexpressed c-Myc in murine skin, particularly in epidermal stem cells.
  • To discuss the involvement of the c-Myc-p21(CIP1) pathway in Ras-driven skin tumorigenesis.

Main Methods:

  • Literature review of studies on c-Myc and Ras in cancer.
  • Focus on murine skin models and epidermal stem cells.
  • Analysis of molecular pathways, including c-Myc-p21(CIP1).

Main Results:

  • Myc and Ras cooperate to promote tumorigenesis by overcoming cell-cycle arrest and apoptosis.
  • Endogenous c-Myc plays a significant role in epidermal stem cells in murine skin.
  • The c-Myc-p21(CIP1) pathway is essential for Ras-driven skin tumor development.

Conclusions:

  • The antagonistic effects of Myc and Ras highlight complex oncogene cooperation in cancer.
  • Targeting the c-Myc-p21(CIP1) pathway may offer therapeutic strategies for Ras-driven cancers.
  • Further research into oncogene interactions is vital for advancing cancer treatment.

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