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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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Initiation of Metastatic Breast Carcinoma by Targeting of the Ductal Epithelium with Adenovirus-Cre: A Novel Transgenic Mouse Model of Breast Cancer
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Direct reprogramming by oncogenic Ras and Myc.

Irene Ischenko1, Jizu Zhi, Ute M Moll

  • 1Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.

Proceedings of the National Academy of Sciences of the United States of America
|February 23, 2013
PubMed
Summary
This summary is machine-generated.

Cancer cells reprogram and dedifferentiate early in malignant transformation. Oncogene-induced plasticity drives this process, enabling cancer stem cells with metastatic potential.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Cancer cell reprogramming and dedifferentiation are observed but not causally linked to cancer.
  • Mechanisms and identity of metastasizing cancer cells remain largely unknown.

Purpose of the Study:

  • To investigate the role of reprogramming and dedifferentiation in cancer initiation and metastasis.
  • To elucidate the mechanisms underlying the generation of metastatic cancer cells.

Main Methods:

  • Utilized a conditional KrasG12D oncogene expression model in primary mouse cells.
  • Reconstructed metastatic conversion in cell culture.
  • Investigated the role of proto-oncogene c-Myc.

Main Results:

  • KrasG12D expression induces reprogramming, dedifferentiation, and acquisition of stem cell characteristics.
  • Proto-oncogene c-Myc controls the generation of self-renewing metastatic cancer cells.
  • Oncogene-induced plasticity enables non-stem cancer cells to dedifferentiate into metastatic cancer stem cells.

Conclusions:

  • Reprogramming and dedifferentiation are fundamental early steps in oncogene-driven cancer initiation.
  • Metastatic conversion is linked to oncogene-induced phenotypic plasticity and c-Myc activity.
  • Disruption of cancer stem cell/non-stem cell equilibrium promotes high metastatic capacity.