Spontaneous Tumors and Common Diseases in Two Colonies of Syrian Hamsters. II. Respiratory Tract and Digestive System2

Pour, Parviz M.; Möhr, U.; Cardesa, Antonio; Althoff, J.; Kmoch, Norbert

doi:10.1093/jnci/56.5.937

Cited by 51 publications

(22 citation statements)

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“…of the hamsters in those studies was not reported. 42,43,57 Therefore, it is possible that spontaneous inflammation and neoplasia that have been historically reported in geriatric hamsters similar to those of our study, may have been associated with helicobacter-induced chronic inflammation.…”

Section: Discussionsupporting

confidence: 72%

Progressive Proliferative and Dysplastic Typhlocolitis in Aging Syrian Hamsters Naturally Infected with Helicobacter spp.: A Spontaneous Model of Inflammatory Bowel Disease

et al. 2006

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Helicobacter spp. have been implicated in a variety of gastrointestinal tract diseases, including peptic ulcer disease, gastric cancer, and inflammatory bowel disease (IBD), in humans and animals. Although most models of IBD are experimentally induced, spontaneous or natural models of IBD are rare. Herein, we describe a long-term study of chronic, progressive lesions that develop in the distal portion of the large bowel of unmanipulated Syrian hamsters naturally infected with Helicobacter spp. Twenty-four Syrian hamsters of three age groups (group A, 1 month [n = 4], group B, 7-12 months [n = 12], group C, 18-24 months [n = 12]), underwent complete postmortem examination. Results of microbial isolation and polymerase chain reaction and restriction fragment length polymorphism analyses confirmed the presence of Helicobacter spp. infection in the distal portion of the large bowel of all animals. Additionally, confounding pathogens, such as Clostridium difficile, Lawsonia intracellularis, and Giardia spp. that can cause proliferative enteritis, were absent in the hamsters of this study. Histopathologic scores for inflammation (P < 0.01), hyperplasia (P < 0.01), and dysplasia (P < 0.05) were significantly higher in the ileocecocolic (ICC) junction of animals in group C, relative to group A. Dysplastic lesions of various grades were detected in 5 of 11 hamsters in group C. Interestingly, the segment of the bowel that is usually colonized by Helicobacter spp. in hamsters had the most severe lesions. One hamster of group C developed a malignant fibrous histiocytoma, whereas another hamster developed a round cell sarcoma originating from the ICC junction. Thus, lesions in the distal portion of the large bowel of aging hamsters naturally colonized with Helicobacter spp. warrants developing the hamster as an animal model of IBD and potentially IBD-related cancer.

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Section: Discussionsupporting

confidence: 72%

Progressive Proliferative and Dysplastic Typhlocolitis in Aging Syrian Hamsters Naturally Infected with Helicobacter spp.: A Spontaneous Model of Inflammatory Bowel Disease

et al. 2006

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“…The incidences of hemangioma and hemangiosarcoma in the vehicle groups in the investigative study were greater than that in the carcinogenicity study and more in line with background incidences of up to 1% in hamster that have been reported previously (Dontenwill et al 1973;Pour et al 1976).…”

Section: Discussionsupporting

confidence: 87%

Tesaglitazar, a Dual PPAR-α/γ Agonist, Hamster Carcinogenicity, Investigative Animal and Clinical Studies

et al. 2011

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Tesaglitazar was developed as a dual peroxisome proliferator-activated receptor (PPARa/g). To support the clinical program, a hamster carcinogenicity study was performed. The only neoplastic findings possibly related to treatment with tesaglitazar were low incidences of hemangioma and hemangiosarcoma in the liver of male animals. A high-power, two-year investigative study with interim necropsies was performed to further elucidate these findings. Treatment with tesaglitazar resulted in changes typical for exaggerated PPARa pharmacology in rodents, such as hepatocellular hypertrophy and hepatocellular carcinoma, but not an increased frequency of hemangiosarcomas. At the highest dose level, there was an increased incidence of sinusoidal dilatation and hemangiomas. No increased endothelial cell (EC) proliferation was detected in vivo, which was confirmed by in vitro administration to ECs. Immunohistochemistry and gene expression analyses indicated increased cellular stress and vascular endothelial growth factor (VEGF) expression in the liver, which may have contributed to the sinusoidal dilatation. A two-fold increase in the level of circulating VEGF was detected in the hamster at all dose levels, whereas no effect on VEGF was observed in patients treated with tesaglitazar. In conclusion, investigations have demonstrated that tesaglitazar does not produce hemangiosarcomas in hamster despite a slight effect on vascular morphology in the liver.

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“…They did, however, note that outbreaks of clinical enteritis were a common occurrence and subclinical infections were suspected in almost all of the animals (3). In a study of a Hannover colony of Syrian hamsters, liver tumors were composed of hemangioendotheliomas (5.6% of all tumors), hepatocellular adenomas (16.7% of all tumors) cholangiocarcinomas (16.7% of all tumors), and cholangiomas (6.1% of all tumors) (37,38). That colony also had a high incidence of intestinal adenocarcinoma with lymphogenic metastasis to the lymphatic and mesenteric lymph nodes.…”

Section: Discussionmentioning

confidence: 99%

Chronic Hepatitis, Hepatic Dysplasia, Fibrosis, and Biliary Hyperplasia in Hamsters Naturally Infected with a Novel Helicobacter Classified in the H. bilis Cluster

et al. 2009

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We recently described helicobacter-associated progressive, proliferative, and dysplastic typhlocolitis in aging (18-to 24-month-old) Syrian hamsters. Other pathogens associated with typhlocolitis in hamsters, Clostridium difficile, Lawsonia intracellularis, and Giardia spp., were not indentified. The presence of Helicobacter genusspecific DNA was noted by PCR in cecal and paraffin-embedded liver samples from aged hamsters by the use of Helicobacter-specific PCR primers. By 16S rRNA analysis, the Helicobacter sp. isolated from the liver tissue was identical to the cecal isolates from hamsters. The six hamster 16S rRNA sequences form a genotypic cluster most closely related to Helicobacter sp. Flexispira taxon 8, part of the Helicobacter bilis/H. cinaedi group. Livers from aged helicobacter-infected hamsters showed various stages of predominantly portocentric and, to a lesser extent, perivenular fibrosis. Within nodules, there was cellular atypia consistent with nodular dysplasia. The livers also exhibited a range of chronic active portal/interface and lobular inflammation, with significant portal hepatitis being present. The inflammation was composed of a mixture of lymphocytes, neutrophils, and macrophages, indicative of its chronic-active nature in these aged hamsters infected with Helicobacter spp. The isolation of novel Helicobacter spp., their identification by PCR from the diseased livers of aged hamsters, and their taxonomic classification as belonging to the Helicobacter bilis cluster strengthen the argument that H. bilis and closely related Helicobacter spp. play an etiological role in hepatobiliary disease in both animals and humans.We recently described progressive, proliferative, and dysplastic typhlocolitis in aging (18-to 24-month-old) Syrian hamsters (31). The lesions in these hamsters were more severe in the older animals aged 7 to 24 months than in the younger, 1-to 6-month-old hamsters. The presence of Helicobacter spp. in the large bowel of all 24 hamsters included in the study was confirmed by culture and Helicobacter-specific PCR (31). Other pathogens associated with typhlocolitis in hamsters, Clostridium difficile, Lawsonia intracellularis, and Giardia spp., were not indentified in this study (31). Enterohepatic Helicobacter spp. are associated with the development of inflammatory bowel disease in mice and, as determined more recently, humans (2, 18, 27, 51). These helicobacters can also induce hepatitis and hepatocellular carcinoma in susceptible strains of mice (1,14,19). We undertook a study to examine in detail the histological profile of the livers of hamsters aged 18 to 24 months and to determine whether Helicobacter sp. DNA was present in their livers (31). In addition, we purchased a small number of 6-month-old hamsters from the same vendor which originally supplied the aged hamsters and examined them for the presence of Helicobacter spp. in their intestines and liver and whether inflammation was associated with the presence of Helicobacter spp. in these target tissues. We document t...

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Spontaneous Tumors and Common Diseases in Two Colonies of Syrian Hamsters. II. Respiratory Tract and Digestive System2

Cited by 51 publications

References 0 publications

Progressive Proliferative and Dysplastic Typhlocolitis in Aging Syrian Hamsters Naturally Infected with Helicobacter spp.: A Spontaneous Model of Inflammatory Bowel Disease

Progressive Proliferative and Dysplastic Typhlocolitis in Aging Syrian Hamsters Naturally Infected with Helicobacter spp.: A Spontaneous Model of Inflammatory Bowel Disease

Tesaglitazar, a Dual PPAR-α/γ Agonist, Hamster Carcinogenicity, Investigative Animal and Clinical Studies

Chronic Hepatitis, Hepatic Dysplasia, Fibrosis, and Biliary Hyperplasia in Hamsters Naturally Infected with a Novel Helicobacter Classified in the H. bilis Cluster

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