PMID- 9806616
OWN - NLM
STAT- MEDLINE
DCOM- 19981120
LR  - 20071114
IS  - 0033-7587 (Print)
IS  - 0033-7587 (Linking)
VI  - 150
IP  - 5 Suppl
DP  - 1998 Nov
TI  - Heavy-ion radiobiology: new approaches to delineate mechanisms underlying 
      enhanced biological effectiveness.
PG  - S126-45
AB  - Shortly after the discovery of polonium and radium by Marie Curie and her husband 
      and colleague, Pierre Curie, it was learned that exposure to these alpha-particle 
      emitters produced deleterious biological effects. The mechanisms underlying the 
      increased biological effectiveness of densely ionizing radiations, including 
      alpha particles, neutrons and highly energetic heavy charged particles, remain an 
      active area of investigation. In this paper, we review recent advances in several 
      areas of the radiobiology of these densely ionizing radiations, also known as 
      heavy ions. Advances are described in the areas of DNA damage and repair, 
      chromosome aberrations, mutagenesis, neoplastic transformation in vitro, genomic 
      instability, normal tissue radiobiology and carcinogenesis in vivo. We focus on 
      technical innovations, including novel applications of pulsed-field gel 
      electrophoresis, fluorescence in situ hybridization (FISH), linkage analysis, and 
      studies of gene expression and protein expression. We also highlight the use of 
      new cellular and animal systems, including those with defined DNA repair 
      deficiencies, as well as epithelial cell model systems to assess neoplastic 
      transformation both in vitro and in vivo. The studies reviewed herein have had a 
      substantial impact on our understanding of the genotoxic effects of heavy ions as 
      well as their distinct effects on tissue homeostasis. The use of these radiations 
      in cancer therapy is also discussed. The use of both heavy-ion and proton therapy 
      is on the upswing in several centers around the world, due to their unique energy 
      deposition characteristics that enhance the therapeutic effect and help reduce 
      damage to normal tissue.
FAU - Blakely, E A
AU  - Blakely EA
AD  - Life Sciences Division, Ernest Orlando Lawrence Berkeley National Laboratory, 
      Berkeley, California 94720, USA.
FAU - Kronenberg, A
AU  - Kronenberg A
LA  - eng
GR  - CA73966/CA/NCI NIH HHS/United States
GR  - EY10737/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Radiat Res
JT  - Radiation research
JID - 0401245
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Animals
MH  - Cell Cycle/radiation effects
MH  - Cell Transformation, Neoplastic/radiation effects
MH  - Chromosome Aberrations
MH  - DNA/radiation effects
MH  - *Heavy Ions
MH  - Humans
MH  - Linear Energy Transfer
MH  - Mutagenesis
MH  - Neoplasms, Radiation-Induced
MH  - *Radiobiology
RF  - 264
OTO - NASA
OT  - NASA Discipline Radiation Health
OT  - Non-NASA Center
FIR - Blakely, E A
IR  - Blakely EA
IRAD- Lawrence Berkeley Lab, CA
FIR - Kronenberg, A
IR  - Kronenberg A
IRAD- Lawrence Berkeley Lab, CA
FIR - Chatterjee, A
IR  - Chatterjee A
IRAD- Lawrence Berkeley Lab, CA
EDAT- 1998/11/07 00:00
MHDA- 1998/11/07 00:01
CRDT- 1998/11/07 00:00
PHST- 1998/11/07 00:00 [pubmed]
PHST- 1998/11/07 00:01 [medline]
PHST- 1998/11/07 00:00 [entrez]
PST - ppublish
SO  - Radiat Res. 1998 Nov;150(5 Suppl):S126-45.