The role of promotion in carcinogenesis from protracted high-LET exposure

Phys Med. 2001:17 Suppl 1:157-60.

Abstract

Recent analysis of epidemiological studies using the two-stage clonal expansion (TSCE) model has shown that radiation-induced promotion dominates radiation-induced initiation for protracted exposures to radon. This strong promotion effect (i.e. enhanced proliferation of already-initiated cells) causes a pronounced 'inverse dose-rate effect', but by a mechanism completely different from those usually discussed in this connection. This rather startling result is discussed along with implications to extended space missions that include a significant amount of high-LET radiation. It is suggested that the effect might be caused by a 'Bystander Effect' by which normal cells in the vicinity of initiated cells are hit by alpha particles and send out signals that modify the cell kinetics of the already-initiated clones.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Aged
  • Alpha Particles*
  • Bystander Effect
  • Cell Transformation, Neoplastic*
  • Dose-Response Relationship, Radiation
  • Humans
  • Linear Energy Transfer*
  • Lung Neoplasms / etiology*
  • Lung Neoplasms / mortality
  • Middle Aged
  • Mining
  • Models, Biological
  • Mutation
  • Neoplasms, Radiation-Induced / etiology*
  • Neoplasms, Radiation-Induced / mortality
  • Radon*
  • Relative Biological Effectiveness
  • Risk

Substances

  • Radon