Biology User Support Team – NASA Space Radiation Laboratory
Paul Wilson heads the Biology Department’s NASA Space Radiation
Laboratory (NSRL) User Support Team. The NSRL facility, operated jointly
with BNL’s Collider-Accelerator and Medical Departments, supplies beams
of high-energy protons and heavy-charged particles used by researchers
from the US and around the world to simulate the effects of space
radiation exposures on biological systems, materials and instruments
pertinent to NASA’s mission objectives. The NSRL Biology User Support
Team consists of scientific, professional and administrative staff
members who provide radiobiology expertise and NSRL facility support to
over 200 NASA-funded researchers worldwide.
- Studying effects of low and high linear
energy transfer (LET) ionizing radiation on
normal, tumor and DNA damage signaling and
repair-deficient cells, tissues, and animal
models over wide ranges of doses and dose rates.
- Identifying links between cellular
radiosensitivity, individual cancer
predisposition, and genetics with a primary
focus on DNA damage response pathways including
DNA damage sensing, signaling, and repair, and
- Developing reliable, high-throughput
phenotype-based radiation biodosimetry assays
using techniques such as combinatorial
immunocytochemistry, molecular cytogenetics, and
novel DNA sensing/amplification technologies;
validating new radiation biodosimetry assays
against “gold-standard” radiobiological assays.
- Assessing population-level functional
variation in biological responses to ionizing
radiation given our inherently large degree of
This research is funded by grants from the U.S. DOE Low
Dose Radiation Research Program and the NASA
Space Radiation Program.
- Wilson P.F., and Bedford J.S.
The Textbook of Radiation Oncology, Third Edition, pp. 1–30, T.L. Phillips,
R.T. Hoppe and M.A. Roach III (eds.), W.B. Saunders Company, Philadelphia, PA (2010).
Wilson P.F., Hinz J.M., Urbin S.S., Nham P.B., and Thompson L.H.
Influence of homologous recombinational repair on cell survival and
chromosomal aberration induction during the cell cycle in gamma-irradiated
DNA Repair, 9(7):737–744 (2010). PubMed
Wilson P.F., Nagasawa H., Fitzek M.M., Little J.B., and Bedford J.S.
G2-phase chromosomal radiosensitivity of primary fibroblasts from hereditary
retinoblastoma family members and some apparently normal controls.
Radiation Research, 173(1):62–70 (2010). PubMed
Wilson P.F., Nham P.B., Urbin S.S., Hinz J.M., Jones I.M., and Thompson L.H.
Inter-individual variation in DNA double-strand break repair in human
fibroblasts before and after exposure to low doses of ionizing radiation.
Mutation Research, 683(1-2):91–97 (2010). PubMed
Kato T.A., Wilson P.F., Nagasawa H., Peng Y., and Bedford J.S.
Variations in radiosensitivity among individuals: a potential impact on risk assessment?
Health Physics, 97(5):470–480 (2009). PubMed
Nagasawa H., Wilson P.F., Chen D.J., Thompson L.H., Bedford J.S., and Little J.B.
Low doses of alpha particles do not induce sister chromatid exchanges in
bystander Chinese hamster cells defective in homologous recombination.
DNA Repair, 7(3):515–522 (2008). PubMed
Wilson P.F., Nagasawa H., Warner C.L., Fitzek M.M., Little J.B., and Bedford J.S.
Radiation sensitivity of primary fibroblasts from hereditary retinoblastoma
family members and some apparently normal controls: colony formation ability
during continuous low-dose-rate gamma irradiation.
Radiation Research, 169(5):483–494 (2008). PubMed
Fan J.S., Wilson P.F., Wong H.-K., Urbin S.S., Thompson L.H., and Wilson D.M. III.
XRCC1 down regulation in human cells leads to DNA damaging agent sensitivity, elevated sister chromatid exchange, and reduced survival of
BRCA2 mutant cells.
Environmental and Molecular Mutagenesis 48(6):491–500 (2007). PubMed
Hinz J.M., Tebbs R.S., Wilson P.F., Nham P.B., Salazar E.P., Nagasawa H., Urbin S.S.,
Bedford J.S., and Thompson L.H.
Repression of mutagenesis by Rad51D-mediated homologous recombination.
Nucleic Acids Research 34(5):1358–1368 (2006). PubMed
Kato T.A., Wilson P.F., Nagasawa H., Fitzek M.M., Weil M.M., Little J.B., and Bedford J.S.
A defect in DNA double strand break processing in cells from unaffected
parents of retinoblastoma patients and other apparently normal humans.
DNA Repair, 6(6):818–829, 2006. PubMed
Nagasawa H., Peng Y., Wilson P.F., Lio Y.-C., Chen D.J., Bedford J.S., and Little J.B.
Role of homologous recombination in the alpha particle bystander effect for
sister chromatid exchanges and chromosomal aberrations.
Radiation Research 164(2):141–147 (2005). PubMed