Strong Signature of Natural Selection within an FHIT Intron Implicated in Prostate Cancer Risk
2008

Natural Selection and Prostate Cancer Risk

Sample size: 200 publication Evidence: high

Author Information

Author(s): Ding Yan, Garrett Larson, Guillermo Rivas, Cathryn Lundberg, Louis Geller, Ching Ouyang, Jeffrey Weitzel, John Archambeau, Jerry Slater, Mary B. Daly, Al B. Benson, John M. Kirkwood, Peter J. O'Dwyer, Rebecca Sutphen, James A. Stewart, David Johnson, Magnus Nordborg, Theodore G. Krontiris

Primary Institution: Division of Molecular Medicine, Beckman Research Institute of the City of Hope, Duarte, California, United States of America

Hypothesis

Does the FHIT intron contain genetic variations that increase the risk of prostate cancer?

Conclusion

The study found strong evidence that specific genetic variations within the FHIT intron are associated with an increased risk of prostate cancer.

Supporting Evidence

  • The study identified multiple SNPs in the FHIT intron that are associated with prostate cancer risk.
  • Strong signatures of natural selection were detected in the FHIT region across different populations.
  • The research refined the association with prostate cancer risk to a 15 kb region within the FHIT intron.

Takeaway

Scientists looked at a part of a gene called FHIT to see if it could make people more likely to get prostate cancer, and they found some clues that it might.

Methodology

The study involved re-sequencing and genotyping a 28.5 kb region around the FHIT gene in prostate cancer cases and controls.

Potential Biases

Potential bias due to the selection of specific populations and the focus on certain SNPs.

Limitations

The study primarily focused on European-American populations, which may limit the generalizability of the findings.

Participant Demographics

200 unrelated patients of European descent affected with prostate cancer and 143 controls of matched ethnicity.

Statistical Information

P-Value

0.00045

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0003533

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