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Intestinal Neoplasia (intestinal + neoplasia)
Selected AbstractsIntestinal Neoplasia in HorsesJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2006S.D. Taylor Background:Intestinal neoplasia of horses is inadequately described. Hypothesis:Intestinal neoplasia of horses has characteristic clinicopathologic features. Animals:Thirty-four horses with intestinal neoplasia. Methods:Retrospective study. Results:Anamnesis, clinical signs, clinicopathologic and pathologic findings in 34 adult horses diagnosed histologically with intestinal neoplasia were reviewed. The horses ranged in age from 2 to 30 years (mean 16.6 years at presentation). The Arabian breed was most represented and there was no sex predisposition. The most common presenting complaints were weight loss, colic, anorexia, and fever. The most consistent clinical signs were poor body condition, tachycardia, tachypnea, fever, and diarrhea. Useful diagnostic tools included rectal examination, routine blood analyses, abdominocentesis, ultrasonographic examination, rectal biopsy, and exploratory laparotomy. Alimentary lymphoma was the most common intestinal neoplasia identified, followed by adenocarcinoma and smooth muscle tumors. The small intestine was the most common segment of intestine affected for all neoplasms. Intestinal neoplasia was diagnosed antemortem in 13 of 34 (38%) horses. The median time from onset of clinical signs to death or euthanasia was 1.9 months. The discharge rate was 15%. Although the longest survival was observed in horses with jejunal adenocarcinoma, all horses were eventually euthanized because of intestinal neoplasia. Conclusions: Arabian horses were 4.5 times more likely to have intestinal neoplasia diagnosed than were other breeds. [source] ApcMin/+ mouse model of colon cancer: Gene expression profiling in tumorsJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 6 2004Daniel Leclerc Abstract The ApcMin/+ mouse is a popular animal model for studies of human colon cancer, but the molecular changes associated with neoplasia in this system have only been partially characterized. Our aim was to identify novel genes involved in tumorigenesis in this model. RNA from intestinal adenomas and from pre-neoplastic small intestine were prepared from six ApcMin/+ mice. The tumor transcriptomes were analyzed with high-density oligonucleotide microarrays representing ,12,000 probe sets; we compared their profiles with those of matched pre-neoplastic intestine. Stringent analysis revealed reproducible changes for 98 probe sets representing 90 genes, including novel observations regarding 50 genes whose involvement in this mouse model has never been reported. In addition to the expected changes in growth regulatory genes, the altered gene products could be assigned to four functional groupings that should enhance tumorigenesis: metabolic changes that would result in a high rate of glycolysis, alterations in enzymes involved in reactive oxygen species or carcinogen metabolism, cytoskeletal elements, and proteins involved in tumor invasion or angiogenesis. A fifth group consisted of expression changes that might restrict tumor progression, suggesting that the adenomatous state reflects a balance of pro- and anti-tumorigenic factors. Since many of the altered genes had not previously been reported to be involved in any tumorigenic processes, our observations provide a host of new candidates for potential modulation to prevent or treat intestinal neoplasia. Supplementary material for this article can be found at http://www.mrw.interscience.wiley.com/suppmat/0730-2312/suppmat/v93.html. © 2004 Wiley-Liss, Inc. [source] Intestinal Neoplasia in HorsesJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2006S.D. Taylor Background:Intestinal neoplasia of horses is inadequately described. Hypothesis:Intestinal neoplasia of horses has characteristic clinicopathologic features. Animals:Thirty-four horses with intestinal neoplasia. Methods:Retrospective study. Results:Anamnesis, clinical signs, clinicopathologic and pathologic findings in 34 adult horses diagnosed histologically with intestinal neoplasia were reviewed. The horses ranged in age from 2 to 30 years (mean 16.6 years at presentation). The Arabian breed was most represented and there was no sex predisposition. The most common presenting complaints were weight loss, colic, anorexia, and fever. The most consistent clinical signs were poor body condition, tachycardia, tachypnea, fever, and diarrhea. Useful diagnostic tools included rectal examination, routine blood analyses, abdominocentesis, ultrasonographic examination, rectal biopsy, and exploratory laparotomy. Alimentary lymphoma was the most common intestinal neoplasia identified, followed by adenocarcinoma and smooth muscle tumors. The small intestine was the most common segment of intestine affected for all neoplasms. Intestinal neoplasia was diagnosed antemortem in 13 of 34 (38%) horses. The median time from onset of clinical signs to death or euthanasia was 1.9 months. The discharge rate was 15%. Although the longest survival was observed in horses with jejunal adenocarcinoma, all horses were eventually euthanized because of intestinal neoplasia. Conclusions: Arabian horses were 4.5 times more likely to have intestinal neoplasia diagnosed than were other breeds. [source] Functional colonography of Min mice using dark lumen dynamic contrast-enhanced MRIMAGNETIC RESONANCE IN MEDICINE, Issue 3 2008C. Chad Quarles Abstract Dark lumen MRI colonography detects colonic polyps by minimization of the intestinal lumen signal intensity. Here we validate the use of perfluorinated oil as an intestinal-filling agent for dark lumen MRI studies in mice, enabling the physiological characterization of colonic polyps by dynamic contrast-enhanced MRI. In control and Min (multiple intestinal neoplasia) mice with and without pretreatment with oral dextran sodium sulfate (DSS), polyps as small as 0.94 mm diameter were consistently identified using standard 2D gradient echo imaging (voxel size, 0.23 × 0.16 × 0.5 mm). In serial studies, polyp growth rates were heterogeneous with an average ,5% increase in polyp volume per day. In DSS-treated control mice the colon wall contrast agent extravasation rate constant, Ktrans, and extravascular extracellular space volume fraction, ve, values were measured for the first time and found to be 0.10 ± 0.03 min,1 and 0.23 ± 0.09, respectively. In DSS-treated Min mice, polyp Ktrans values (0.09 ± 0.04 min,1) were similar to those in the colon wall but the ve values were substantially lower (0.16 ± 0.03), suggesting increased cellular density. The functional dark-lumen colonography approach described herein provides new opportunities for the noninvasive assessment of gastrointestinal disease pathology and treatment response in mouse models. Magn Reson Med 60:718,726, 2008. © 2008 Wiley-Liss, Inc. [source] APC-dependent regulation of ornithine decarboxylase in human colon tumor cellsMOLECULAR CARCINOGENESIS, Issue 1 2002Kimberly E. Fultz Abstract Mutation/deletion of the adenomatous polyposis coli (APC) tumor suppressor gene in germline cells of rodents and humans is associated with increased intestinal activity of ornithine decarboxylase (ODC), the first enzyme in polyamine synthesis, and intestinal neoplasia. To study the role of APC in signaling ODC expression, we used the human colon tumor cell line HT29 (wtAPC,/,), which has been stably transfected with a zinc-inducible wild-type APC gene. The addition of ZnCl2 to HT29-APC cells increased wild-type APC protein and Mad1 RNA and protein and decreased levels of c- myc and ODC RNA and protein, relative to these parameters in HT29 cells transfected with the same plasmid containing the ,-galactosidase gene in place of APC. Upon induction of APC expression, ODC promoter activity and RNA levels were suppressed. When the e-box domain in the 5, flanking region of the ODC gene was mutated, ODC promoter activity was unaffected by wild-type APC expression. Antisense, but not missense, c- myc oligonucleotides decreased ODC activity in HT29 cells expressing mutant APC. These results demonstrated that wild-type APC suppressed c-myc and activated Mad1 expression in HT29 colon-derived cells. These proteins, in turn, regulated the transcription of target genes, including ODC. The data presented indicate that ODC is a modifier of APC-dependent signaling in intestinal cells and tissues. © 2002 Wiley-Liss, Inc. [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] | ||||||||||