Mechanisms of disseminated cancer cell dormancy: an awakening field

Nat Rev Cancer. 2014 Sep;14(9):611-22. doi: 10.1038/nrc3793. Epub 2014 Aug 14.


Metastases arise from residual disseminated tumour cells (DTCs). This can happen years after primary tumour treatment because residual tumour cells can enter dormancy and evade therapies. As the biology of minimal residual disease seems to diverge from that of proliferative lesions, understanding the underpinnings of this new cancer biology is key to prevent metastasis. Analysis of approximately 7 years of literature reveals a growing focus on tumour and normal stem cell quiescence, extracellular and stromal microenvironments, autophagy and epigenetics as mechanisms that dictate tumour cell dormancy. In this Review, we attempt to integrate this information and highlight both the weaknesses and the strengths in the field to provide a framework to understand and target this crucial step in cancer progression.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Autophagy
  • Epigenesis, Genetic
  • Humans
  • Neoplasm, Residual / pathology
  • Neoplasms / genetics
  • Neoplasms / immunology
  • Neoplasms / metabolism
  • Neoplasms / pathology*
  • Neovascularization, Pathologic / immunology
  • Signal Transduction
  • Stress, Physiological
  • Tumor Microenvironment