Show simple item record

dc.contributor.authorWilson, James W
dc.contributor.authorPotten, Christopher S
dc.date.accessioned2009-11-13T15:32:02Z
dc.date.available2009-11-13T15:32:02Z
dc.date.issued2000-08-15
dc.identifier.citationThe effect of exogenous prostaglandin administration on tumor size and yield in Min/+ mice. 2000, 60 (16):4645-53 Cancer Res.en
dc.identifier.issn0008-5472
dc.identifier.pmid10969819
dc.identifier.urihttp://hdl.handle.net/10541/86148
dc.description.abstractThis study set out to examine the effect of exogenous prostaglandin (PG) administration on tumor development in Min/+ mice. Mice were treated with the stable prostaglandin E2 analogue 16,16-dimethyl-PGE2 from 6-18 weeks of age. Mice were sacrificed, and tumor burden was assessed using morphometric techniques. Parameters measured were median tumor size, mean tumor size, the proportion of the area of the gastrointestinal mucosa covered with tumor, and the number of tumors per 1000 mm2 of gastrointestinal mucosa. In addition, proliferative and apoptotic indices were determined. These measurements were carried out for all regions of the small intestine (i.e., duodenum, jejunum, upper ileum, and lower ileum) and the large intestine (i.e., cecum and mid-colon/rectum). 16,16-Dimethyl-PGE2-treated animals showed a significant decrease in tumor burden (by approximately 50-70%), in comparison with those animals that were treated with vehicle alone (0.001% ethanol in 0.9% sterile saline), in all regions of the intestine (at P = 0.008 or better). This effect was contributed to by a reduction in the number of tumors (by approximately 20-50%) and a reduction in tumor size (by approximately 10-70%). An increase in tumor cell turnover was associated with this decrease in tumor burden, as determined by the changes in the levels of thymidine incorporation (significant at P = 0.003), apoptosis, and mitosis (nonsignificant).
dc.language.isoenen
dc.subjectDuodenal Canceren
dc.subjectIleal Canceren
dc.subjectIntestinal Canceren
dc.subject.mesh16,16-Dimethylprostaglandin E2
dc.subject.meshAnimals
dc.subject.meshApoptosis
dc.subject.meshCell Cycle
dc.subject.meshCyclin-Dependent Kinase Inhibitor p21
dc.subject.meshCyclins
dc.subject.meshDuodenal Neoplasms
dc.subject.meshFemale
dc.subject.meshGenetic Predisposition to Disease
dc.subject.meshIleal Neoplasms
dc.subject.meshIntestinal Mucosa
dc.subject.meshIntestinal Neoplasms
dc.subject.meshMale
dc.subject.meshMice
dc.subject.meshMice, Inbred C57BL
dc.subject.meshMitosis
dc.subject.meshThymidine
dc.titleThe effect of exogenous prostaglandin administration on tumor size and yield in Min/+ mice.en
dc.typeArticleen
dc.contributor.departmentSection of Cell and Tumour Biology, Paterson Institute for Cancer Research, Manchester, United Kingdom. jwilson@picr.man.ac.uken
dc.identifier.journalCancer Researchen
html.description.abstractThis study set out to examine the effect of exogenous prostaglandin (PG) administration on tumor development in Min/+ mice. Mice were treated with the stable prostaglandin E2 analogue 16,16-dimethyl-PGE2 from 6-18 weeks of age. Mice were sacrificed, and tumor burden was assessed using morphometric techniques. Parameters measured were median tumor size, mean tumor size, the proportion of the area of the gastrointestinal mucosa covered with tumor, and the number of tumors per 1000 mm2 of gastrointestinal mucosa. In addition, proliferative and apoptotic indices were determined. These measurements were carried out for all regions of the small intestine (i.e., duodenum, jejunum, upper ileum, and lower ileum) and the large intestine (i.e., cecum and mid-colon/rectum). 16,16-Dimethyl-PGE2-treated animals showed a significant decrease in tumor burden (by approximately 50-70%), in comparison with those animals that were treated with vehicle alone (0.001% ethanol in 0.9% sterile saline), in all regions of the intestine (at P = 0.008 or better). This effect was contributed to by a reduction in the number of tumors (by approximately 20-50%) and a reduction in tumor size (by approximately 10-70%). An increase in tumor cell turnover was associated with this decrease in tumor burden, as determined by the changes in the levels of thymidine incorporation (significant at P = 0.003), apoptosis, and mitosis (nonsignificant).


This item appears in the following Collection(s)

Show simple item record