gms | German Medical Science

MAINZ//2011: 56. GMDS-Jahrestagung und 6. DGEpi-Jahrestagung

Deutsche Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie e. V.
Deutsche Gesellschaft für Epidemiologie e. V.

26. - 29.09.2011 in Mainz

PTGS1 and PTGS2 polymorphisms, fatty acid intake, and risk of colon and rectal cancer

Meeting Abstract

  • Nina Habermann - NCT/DKFZ, Heidelberg
  • Martha L. Slattery - University of Utah, Salt Lake City
  • Elizabeth M. Poole - Harvard Medical School/Harvard School of Public Health, Boston
  • Liren Xiao - Fred Hutchinson Cancer Research Center, Seattle
  • Rachel Galbraith - Fred Hutchinson Cancer Research Center, Seattle
  • David Duggan - Translational Genomics Research Institut, Phoenix
  • Richard J. Kulmacz - University of Texas Health Science Center at Houston, Houston
  • Bette J. Caan - Kaiser Permanente Medical Research Program, Oakland
  • Lisl Koepl - Fred Hutchinson Cancer Research Center, Seattle
  • Anne Coghill - Fred Hutchinson Cancer Research Center, Seattle
  • Karen W. Makar - Fred Hutchinson Cancer Research Center, Seattle
  • Abbie Lundgreen - Fred Hutchinson Cancer Research Center, Seattle
  • John Potter - Fred Hutchinson Cancer Research Center, Seattle
  • Cornelia Ulrich - NCT/DKFZ, Heidleberg

Mainz//2011. 56. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds), 6. Jahrestagung der Deutschen Gesellschaft für Epidemiologie (DGEpi). Mainz, 26.-29.09.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. Doc11gmds338

DOI: 10.3205/11gmds338, URN: urn:nbn:de:0183-11gmds3382

Veröffentlicht: 20. September 2011

© 2011 Habermann et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Introduction: Inflammation plays a major role in colorectal cancer. COX-1 and COX-2 convert n-3 and n-6 fatty acids into prostaglandins which have anti- and pro-inflammatory effects, respectively [1]. We examined potential interactions between polymorphisms in PTGS1 (COX-1) and PTGS2 (COX-2) and fat and fatty acid (FA) intake in relation to colon and rectal cancer risk.

Methods: A linkage-disequilibrium-based tagSNP-selection algorithm (r2=0.90, MAF=4%) identified tagSNPs in PTGS1 and PTGS2. We genotyped 16 SNPs in PTGS1 and 17 SNPs in PTGS2 on the same Illumina platform in two independent study populations (colon cancer: 1502 cases, 1862 controls; rectal cancer 713 cases, 914 controls). We investigated potential interactions with intake of total fat, saturated FA (SFA), monounsaturated FA (MUFA), polyunsaturated FA (PUFA), arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) on risk of colon or rectal cancer.

Results: We observed several statistically significant interactions between PTGS1 and PTGS2 genotypes and fat and FA intake (Table). However, few interactions were consistent across fat variables and fell into three general categories of associations: a) individuals with the variant allele and low intake of total fat, SFA, or MUFA were at increased risk for rectal cancer (PTGS1 rs10306122-G, p int=0.01-0.01; PTGS2 rs4648268-A; p int=0.01-0.02); b) individuals with the variant allele and high EPA and DHA intake were less likely to develop colon cancer (PTGS1 rs10306110-G, p int=0.003-0.006); and c) individuals with the wildtype genotype and high EPA and DHA intake had stronger protection from colon cancer (PTGS2 rs4648310-A, p int=0.01-0.05). No interactions were observed for AA.

Conclusion: Our study provides some evidence that genetic variability in PTGS1 and PTGS2 and intake of total fat, SFA, or MUFA and EPA or DHA may interact in causing rectal and colon cancer, respectively.


References

1.
Ulrich CM, Bigler J, Potter JD. Non-steroidal anti-inflammatory drugs for cancer prevention: promise, perils and pharmacogenetics. Nat Rev Cancer. 2006;6:130-40.