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| Status |
Public on Oct 07, 2009 |
| Title |
Diet Synergistically Affects Helicobacter pylori-Induced Gastric Carcinogenesis in Nonhuman Primates |
| Organism |
Macaca mulatta |
| Experiment type |
Expression profiling by array
|
| Summary |
BACKGROUND & AIMS: Gastric cancer results from a combination of Helicobacter pylori (H pylori) infection, exposure to dietary carcinogens, and predisposing genetic make-up. Because the role of these factors in gastric carcinogenesis cannot be determined readily in human beings, the present study examined the role of an oral carcinogen and H pylori infection in rhesus monkeys.
METHODS: Gastroscopies were performed in 23 monkeys assigned to 4 groups: controls; nitrosating carcinogen ethyl-nitro-nitrosoguanidine administration alone; and inoculation of a virulent H pylori strain alone (H), or in combination with ethyl-nitro-nitrosoguanidine (EH). Follow-up gastroscopies and biopsies were performed at 3-month intervals for 5 years for pathologic and molecular studies.
RESULTS: Postinoculation, H and EH groups showed persistent infection and antral gastritis. Starting at 2 and 5 years, respectively, gastric intestinal metaplasia and intraepithelial neoplasia developed in 3 EH monkeys but in no other groups. Transcriptional analysis of biopsies at 5 years revealed group-specific expression profiles, with striking changes in EH monkeys, plus a neoplasia-specific expression profile characterized by changes in multiple cancer-associated genes. Importantly, this neoplastic profile was evident in nonneoplastic mucosa, suggesting that the identified genes may represent markers preceding cancer.
CONCLUSIONS: Gastric intraglandular neoplasia is induced in primates when H pylori infection is associated with consumption of a carcinogen similar to the nitrosaminesfound in pickled vegetables, suggesting that H pylori and the carcinogen synergistically induce gastric neoplasia in primates. Monkey arrays used for analysis of the affect of Helicobacter pylori and diet on development of gastric cancer. Each RNA was hybridized against a common reference. Biopsy numbers represent the following in terms of descriptions used in publication of the paper... Each set of numbers/descriptions is organized in the following order:
Biopsy#; Monkey#; Group Code on Fig 5
Biopsy #4674; AB24; E; E1
Biopsy #4684; 16G; E; E2
Biopsy #4716; 89G; H; H1
Biopsy #4724; 54H; H; H2
Biopsy #4720; 20G; H; H3
Biopsy #4710; 92F; C; C1
Biopsy #4714; 26G; C; C2
Biopsy #4712; 92G; C; C3
Biopsy #4726; 08G; H; H4
Biopsy #4722; 57G; H; H5
Biopsy #4718; 85G; H; H6
Biopsy #4694; 48H; HE NON; HE1
Biopsy #4686; 59H; HE NON; HE2
Biopsy #4690; 81G; HE NEO; HE3
Biopsy #4696; 36G; HE NEO; HE4
Biopsy #4692; 63G; HE NEO; HE5
Biopsy #4680; 76G; E; E3
Biopsy #4682; 52G; E; E4
Biopsy #4678; 15G; E; E5
Biopsy #4676; 93G; E; E6
Biopsy #4688; 47H; HE NON; HE6
A pathogenicity experiment design type is where an infective agent such as a bacterium, virus, protozoan, fungus etc. infects a host organism(s) and the infective agent is assayed.
Infection: Rhesus monkeys were infected with H. pylori (+/-)
Compound Based Treatment: Rhesus monkeys were treated with ENNG (N-ethyl-N-nitrosoguanidine) (+/-)
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| Overall design |
pathogenicity_design
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| Contributor(s) |
Merrell DS |
| Citation(s) |
19622359 |
| Submission date |
Oct 06, 2009 |
| Last update date |
Mar 21, 2012 |
| Organization |
Stanford Microarray Database (SMD) |
| E-mail(s) |
array@genome.stanford.edu
|
| Phone |
650-498-6012
|
| URL |
http://genome-www5.stanford.edu/
|
| Department |
Stanford University, School of Medicine
|
| Street address |
300 Pasteur Drive
|
| City |
Stanford |
| State/province |
CA |
| ZIP/Postal code |
94305 |
| Country |
USA |
| |
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| Platforms (1) |
| GPL9360 |
SMD Print_1597 Macaca mulatta |
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| Samples (21)
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| Relations |
| BioProject |
PRJNA118235 |
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