Julie Parsonnet
Grant Building, Room S 156, Stanford University, Stanford, CA 94305-5107
(Tel: 650-725-4561 Fax: 650-725-3584 Email: parsonnt@leland.stanford.edu )
Four factors appear to be important in determining why some people with H. pylori infection get cancer whereas others do not. These factors--in descending order of quality of evidence--are: bacterial genetics, exposure to environmental cofactors for cancer, host genetics, and possibly age at acquisition of infection. For bacterial genetics, it is clear that not all H. pylori are alike. Organisms that harbor the Cag pathogenicity island (PAI) appear to engender the highest risk for adenocarcinoma. This enhanced carcinogenicity may relate to the greater inflammation and cell destruction induced by PAI-containing strains or it may be the direct consequence of bacterial action on host cells. Putative cofactors for cancer include dietary factors (both protective and harmful) and co-infections. To date, data definitively establishing either of these as important cofactors in H. pylori-related carcinogenesis are lacking. It is likely that host genetic polymorphisms also play a role in H. pylori-related malignancy. The gene that has received the most attention is IL- 1. In one study, variability in this gene appeared to correlate with risk for malignancy. Finally, some speculate that people infected at a young age are at highest risk for cancer. This last hypothesis is difficult to prove epidemiologically.
H. pylori may be responsible for 80% of distal stomach cancers, the second leading cause of cancer death worldwide. Identifying cofactors-for H. pylori-associated cancers will both assist us in determining the most cost-effective strategies for disease prevention and will also point the way to understanding a panoply of inflammation related cancers.
References:
1.Parsonnet J:, Friedman GD, Vandersteen DT, Chang Y, Vogelman JH, Orentreich N, Sibley R. Helicobater pylori infection and risk for gastric cancer. N Engl J Med 1991;325:1127-1131.
2. Parsonnet J, Hansen S, Rodriguez L, Gelb AB,Warnke RA, Jellum E, Orentreich N, Vogelman JH, Friedman GD. Helicobater pylori infection and gastric lymphoma. N Engl J Med 1994;330:1267-1271.
3. Replogle ML, Kasumi W, Ishikawa KB, Yang S, JujiT, Miki K, Parsonnnet J. Increased risk of Helicobater pylori associated with birth in wartime Japan. Int J Epidemiol 1996;25:210-214.
4. Parsonnet J, Harris RA, Hack HM, Owens DK. Cost-effectiveness H Pylori screening to prevent gastric adenocarcinoma: a mandate for clinical trials. Lancet 1 996;348:150-154.
5. Parsonnet J:, Friedman GD, Orentreich N, Vogelman JH. Infection with the CagA-expressing Helicobacter pylori increases risk for gastric cancer. Gut 1997;40;297-301.
6.Parsonnet J:, Shmuely H, Haggerty T. Fecal and oral shedding of Helicobacter pylori from healthy, infected adults. JAMA. 1999;282:2240-45.
7. Rupnow MFT, Shachter RD, Owens DK, Parsonnet J:. Using a dynamic transmission model to predict the future of H. pylori and associated diseases. Emerging Infect Dis 2000;6:228-37.
Julie Parsonnet 1979 A.B. Harvard University, Cambridge, MA
1983 M.D. Cornell University Medical College, NY, NY
1986 Resident Massachusetts General Hospital, Boston, MA
1987 Fellow Massachusetts General Hospital, Boston, MA
Employment
1987-1989 Centers for Disease Control, Epidemic Intelligence Service Officer, Enteric Diseases Branch
1989-1996 Stanford University, Assistant Professor of Medicine (Infectious Diseases and Geographic Medicine)
1992-1996 Stanford University, Assistant Professor of Health Research and Policy (Epidemiology)
1996-1997 Stanford University, Acting Chief, Division of Infectious Diseases and Geographic Medicine.
1996-Stanford University, Associate Professor of Medicine and of Health Research and Policy 1999- Stanford University, Chief, Division of Infectious Diseases and Geographic Medicine