Dormant tumors awaken by a short-term angiogenic burst: The spike hypothesis

Stefano Indraccolo, Elena Favaro, Alberto Amadori

Research output: Contribution to journalArticlepeer-review


Tumor dormancy, a complex and still poorly understood phenomenon observed both in experimental models and in patients, has been associated with insufficient angiogenic capacity. A defined event, termed "angiogenic switch" and characterized by an imbalance between pro- and anti-angiogenic factors, often marks interruption of the dormant state, thus triggering invasive tumor growth. In our current view, sustained angiogenesis is considered essential in promoting this transition. Recently, we demonstrated that coadministration of proliferation-arrested Kaposi's sarcoma cells or recombinant angiogenic factors interrupts dormancy of poorly angiogenic leukemia cells by providing a brief angiogenic burst. These findings indicate that even a transient angiogenic switch can prime progressive tumor growth and suggest that tumor angiogenesis is a process requiring a higher amount of angiogenic factors for its induction than maintenance. Here we discuss the implications of these observations on our view of tumor angiogenesis and on the therapeutic potential of angiogenesis inhibitors.

Original languageEnglish
Pages (from-to)1751-1755
Number of pages5
JournalCell Cycle
Issue number16
Publication statusPublished - Aug 15 2006


  • Angiogenesis
  • bFGF
  • Dormancy
  • Endothelial cell
  • Leukemia
  • VEGF

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology


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