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At least 163 records · Page 9Linked to original sources
PubMed1980

Endoscopic detection of experimentally induced colonic neoplasms in guinea pigs (Cavia porcellus).

Colonoscopic examination was performed daily on 18 normal guinea pigs for 7 weeks and on 27 guinea pigs after 24-35 weeks of biweekly intrarectal instillation of the chemical carcinogen methylnitrosourea. Four normal guinea pigs died during the first 2 weeks of the study, two from colonic perforations and two from cecal bloating due to excessive air insufflation. The other 14 normal animals remained clinically healthy and had no gross abnormalities at the end of the 7-week study. Colonic tumors were detected by colonoscopy in five of seven treated guinea pigs that had grossly visible nodular tumors on the mucosal surface of surgically resected colonic tissue. In another treated guinea pig, a tumor was detected by colonoscopy which was not confirmed grossly. In an additional two treated guinea pigs, tumors were visualized by colonoscopy which could not be demonstrated in surgically resected tissue because of their inaccessible location within the pelvic canal. At necropsy, these latter two guinea pigs had nodular, mucosal growths in the pelvic portion of the colon as indicated by colonoscopy. Microscopically, an additional 13 cases of colonic neoplasms were identified in the resected colonic tissue without gross or colonoscopic evidence of intralumenal nodular growth.

Animals↗
PubMed1999

Intraarterial delivery of adenovirus vectors and liposome-DNA complexes to experimental brain neoplasms.

This study investigated the intraarterial delivery of genetically engineered replication-deficient adenovirus vectors (AVs) and cationic liposome-plasmid DNA complexes (lipoDNA) to experimental brain tumors. Adenovirus or lipoDNA was injected into the internal carotid artery (ICA) of F344 rats harboring intracerebral 9L gliosarcomas, using bradykinin (BK) to selectively permeabilize the blood-tumor barrier (BTB). Brain and internal organs of the animals were collected 48 hr after vector injection and stained for expression of the marker gene product, beta-galactosidase (beta-Gal). Intracarotid delivery of AV to 9L rat gliosarcoma without BTB disruption resulted in transgene expression in 3-10% of tumor cells distributed throughout the tumor. Virus-mediated expression of beta-gal gene products in this tumor model was particularly high in small foci (< or = 0.5 mm), which had invaded the normal brain tissue surrounding the main tumor mass. In these foci more than 50% of tumor cells were transduced. BK infusion increased the amount of transgene-expressing cells in larger tumor foci to 15-30%. In the brain parenchyma only a few endothelial cells expressed beta-gal owing to AV-mediated gene transfer. Intracarotid delivery of lipoDNA bearing a cytoplasmic expression cassette rendered more than 30% of the tumor cells positive for the marker gene without BTB disruption. The pattern of distribution was in general homogeneous throughout the tumor. BK infusion was able to increase further the number of transduced tumor cells to more than 50%. Although lipoDNA-mediated gene transfer showed increased efficacy as compared with AV-mediated gene transfer, it had less specificity since a larger number of endothelial and glial cells also expressed the transgene. AV and lipoDNA injections, in the absence and presence of BK, also resulted in transduction of peripheral organs. AV showed its known predilection for liver and lung. In the case of lipoDNA, parenchymal organs such as liver, lung, testes, lymphatic nodes, and especially spleen, were transduced. These findings indicate that intracarotid application of AV and lipoDNA vectors can effectively transduce tumor cells in the brain, and that BTB modulation by BK infusion can further increase the number of transgene-expressing tumor cells.

Adenoviridae↗
PubMed1980

In vivo-in vitro tumour cell lines: characteristics and limitations as models for human cancer.

In vivo-in vitro tumour cell lines are widely used to study the biology of cancer and to examine the factors influencing the response of tumours to therapeutic agents and regimens. The existing in vivo-in vitro tumours form a uniform and artificial population of experimental neoplasms, with biological characteristics which limit the acceptability of any of these tumours or panel of these tumours as an accurate model for human cancer. All are rapidly growing, transplanted tumours in highly inbred rodents. All have growth rates, cell proliferation patterns and tumour-host interactions different from those of primary tumours in animals or man. Most are immunogenic. Most are anaplastic sarcomas: few are carcinomas; none are well differentiated. The biological differences between in vivo-in vitro tumours and human neoplasms must be considered when the experimental systems are used as models for human cancer.

Animals↗