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Intestinal Polyps (intestinal + polyp)
Selected AbstractsFood Restriction Inhibits the Growth of Intestinal Polyps in Multiple Intestinal Neoplasia MouseCANCER SCIENCE, Issue 3 2002Masakazu Kakuni The effect of food restriction (FR) on spontaneous intestinal carcinogenesis in multiple intestinal neoplasia (Min) mice was examined. Thirty male Min mice were allotted to ad libitum feeding control and 20% FR groups from six weeks of age until the end of the 13-week experimental period. Although the total number of visible intestinal polyps in the FR group was not significantly different from the control group value, a significant decrease in large-sized polyps (>2 mm) and an increase in small-sized polyps (>2 mm) were observed in the distal small intestine. In this segment, the percentage of apoptotic cells counted in intestinal polyps in the FR group was significantly higher than in the control group, the percentage of proliferating cell nuclear antigen (PCNA)-positive cells not being significantly different. These results indicate that the FR may inhibit the growth of intestinal polyps in the Min mouse, and that apoptosis contributed in part to the inhibitory effect. [source] Congenital intestinal polyp associated with intussusception in a 3-day-old foalEQUINE VETERINARY EDUCATION, Issue 3 2006J. R. Gold First page of article [source] Dextran sodium sulfate strongly promotes colorectal carcinogenesis in ApcMin/+ mice: Inflammatory stimuli by dextran sodium sulfate results in development of multiple colonic neoplasmsINTERNATIONAL JOURNAL OF CANCER, Issue 1 2006Takuji Tanaka Abstract The mouse model for familial adenomatous polyposis, ApcMin/+ mouse, contains a truncating mutation in the Apc gene and spontaneously develops numerous adenomas in the small intestine but few in the large bowel. Our study investigated whether dextran sodium sulfate (DSS) treatment promotes the development of colonic neoplasms in ApcMin/+ mice. ApcMin/+ and Apc+/+ mice of both sexes were exposed to 2% dextran sodium sulfate in drinking water for 7 days, followed by no further treatment for 4 weeks. Immunohistochemistry for cyclooxygenase-2, inducible nitric oxide synthase, ,-catenin, p53, and nitrotyrosine, and mutations of ,- catenin and K- ras and loss of wild-type allele of the Apc gene in the colonic lesions were examined. Sequential observation of female ApcMin/+ mice that received DSS was also performed up to week 5. At week 5, numerous colonic neoplasms developed in male and female ApcMin/+ mice but did not develop in Apc+/+ mice. Adenocarcinomas developed in ApcMin/+ mice that received DSS showed loss of heterozygosity of Apc and no mutations in the ,- catenin and K- ras genes. The treatment also significantly increased the number of small intestinal polyps. Sequential observation revealed increase in the incidences of colonic neoplasms and dysplastic crypts in female ApcMin/+ mice given DSS. DSS treatment increased inflammation scores, associated with high intensity staining of ,-catenin, cyclooxygenase-2, inducible nitric oxide synthase and nitrotyrosine. Interestingly, strong nuclear staining of p53 was specifically observed in colonic lesions of ApcMin/+ mice treated with DSS. Our results suggest a strong promotion effect of DSS in the intestinal carcinogenesis of ApcMin/+ mice. The findings also suggest that strong oxidative/nitrosative stress caused by DSS-induced inflammation may contribute to the colonic neoplasms development. © 2005 Wiley-Liss, Inc. [source] Relationships between intestinal polyp formation and fatty acid levels in plasma, erythrocytes, and intestinal polyps in Min miceCANCER SCIENCE, Issue 12 2008Kiyonori Kuriki We have reported that a hyperlipidemic state is characteristic of Apc -deficient Min mice with multiple intestinal polyps. In our earlier case-control study, colorectal cancer risk showed positive relationships with erythrocyte membrane compositions of palmitic and oleic acids, but negative links with linoleic and arachidonic acids. To examine the roles of fatty acids in intestinal polyp formation, levels in plasma, erythrocytes, and intestinal polyps in Min mice were compared with those in wild-type mice. A diet free of eicosapentaenoic and docosahexaenoic acids with antineoplastic effects was fed to all mice from 6 to 15 weeks of age. Fatty acid levels were measured using accelerated solvent extraction and gas,liquid chromatography. Min mice with a hyperlipidemic state and multiple intestinal polyps had elevated values for palmitic and oleic acids in plasma and erythrocytes (at least P < 0.05), and higher plasma level of linoleic acid (P < 0.05). Arachidonic acid was 24.5% lower in erythrocytes (P < 0.0005), but did not differ in plasma. In Min mice, moreover, oleic and arachidonic acids were 1.78 and 1.43 times higher, respectively, in intestinal polyps than in paired normal mucosa (P < 0.05 and P < 0.01, respectively), but linoleic acid was 31.9% lower (P < 0.001). The present study suggests that palmitic, oleic, and arachidonic acids play key roles in intestinal polyp formation, and demonstrates reduced erythrocyte arachidonic acid values of Min mice, in line with our previous findings for patients with sporadic colorectal cancers. (Cancer Sci 2008; 99: 2410,2416) [source] Food Restriction Inhibits the Growth of Intestinal Polyps in Multiple Intestinal Neoplasia MouseCANCER SCIENCE, Issue 3 2002Masakazu Kakuni The effect of food restriction (FR) on spontaneous intestinal carcinogenesis in multiple intestinal neoplasia (Min) mice was examined. Thirty male Min mice were allotted to ad libitum feeding control and 20% FR groups from six weeks of age until the end of the 13-week experimental period. Although the total number of visible intestinal polyps in the FR group was not significantly different from the control group value, a significant decrease in large-sized polyps (>2 mm) and an increase in small-sized polyps (>2 mm) were observed in the distal small intestine. In this segment, the percentage of apoptotic cells counted in intestinal polyps in the FR group was significantly higher than in the control group, the percentage of proliferating cell nuclear antigen (PCNA)-positive cells not being significantly different. These results indicate that the FR may inhibit the growth of intestinal polyps in the Min mouse, and that apoptosis contributed in part to the inhibitory effect. [source] |