Resistance to hepatocarcinogenesis in copenhagen rats. by Geoffrey Albert Wood Download PDF EPUB FB2
Mieritance of resistance to hepatocarcinogenesis in Copenhagen rats Abstract Introduction Materiais and MethodsResuks Discussion References Cha~ter 5. Matrix metaNoproteinases-2 and 9 do not play a role in the growth ofpreneoplastic liver lesions in F rats.
Abstract Introduction 5 Materials and Methods Author: Geoffrey Albert Wood. In the current study, we show that T-cells are also not involved in the resistance of Cop rats to hepatocarcinogenesis.
Cop×nude F2 rats are highly resistant to the growth of GST positive liver lesions initiated with DEN and promoted with the RH protocol. Furthermore, there was no difference in the level of resistance of nude and non-nude by: 4.
Cop rats were crossed with an athymic (nude) rat to produce F1s that were then interbred to produce F2 animals, some of which were nude with a partial Cop background. A comparison of the susceptibility of nude F2 animals and their euthymic (non-nude) littermates allowed us to determine what role, if any, T-cells play in Cop by: 4.
Copenhagen (Cop) rats are completely resistant to the chemical induction of mammary adenocarcinomas, but their susceptibility to hepatocarcinogenesis is virtually unknown, Rat liver is a. grantor: University of Toronto.
TSpace. TSpace is a free and secure research repository established by University of Toronto Libraries to disseminate and preserve the scholarly record of University of : Geoffrey Albert Wood. Cop and DRH rats share several characteristics in their resistance to preneoplastic liver lesion growth and this study, therefore, was designed to examine whether T-cells play a role in Cop resistance.
Cop rats were crossed with an athymic (nude) rat to produce F1s that were then interbred to produce F2 animals, some of which were nude with a partial Cop by: 4. Cop and CFF1 rats exhibit resistance to hepatocarcinogenesis, associated with high rates of remodeling of neoplastic lesions.
We have mapped hepatocarcinogenesis susceptibility, resistance and remodeling loci affecting the number, volume and volume fraction of neoplastic nodules induced by the resistant hepatocyte model in male CFF2 by: The DRH is an inbred rat strain highly resistant to chemically induced hepatocarcinogenesis.
Two clusters of resistance loci Drh1 and Drh2 on chromoso Cited by: 2. Inheritance of resistance to promotion of preneoplastic liver lesions in Copenhagen rats.
G A Wood Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada M5S 3E2. Genetic resistance to hepatocarcinogenesis in the DRH strain rats is primarily dictated by two QTLs. Both Drh1 and Drh2 suppress the number, size and GST-P mRNA expression of the preneoplastic lesion EAF, Drh2 has been shown to suppress later progression of EAF to HCC as well.
Their functions are semi-dominant, as (DRH x F)F1 rats were resistant to hepatocarcinogenesis by 3′ by: 2. These results suggest that the BN rat strain is resistant to hepatocarcinogenesis and that its resistance is genetically transmitted as a dominant character to F1 hybrids of the BN strain with the.
Copenhagen (Cop) rats are completely resistant to the chemical induction of mammary adenocarcinomas, but their susceptibility to hepatocarcinogenesis is virtually unknown.
Rat liver is a well-characterized and easily manipulated tissue in which to study by: Induction of altered hepatic foci in rats by the administration of hypolipidemic peroxisome proliferators alone or following a single dose of diethylnitrosamine.
Cancer Res. Sep; 46 (9)– Dragan YP, Pitot HC. The role of the stages of initiation and promotion in phenotypic diversity during hepatocarcinogenesis in the by: Role of resistant Drh1 locus in chemical carcinogen-induced hepatocarcinogenesis in rats: Analysis with a speed congenic strain Hongbo Liu 1, Ken Higashi 1 and.
Pelz HJ, Hänisch D, Lauenstein G () Resistance to anticoagulant rodenticides in Germany and future strategies to control Rattus norvegicus. Pestic Sci –67 CrossRef Google Scholar Pelz HJ, Rost S, Hunerberg M, Fregin A, Heiberg AC, Baert K, MacNicoll AD, Prescott CV, Walker AS, Oldenburg J, Muller CR () The genetic basis of Cited by: 3.
affect DRH resistance to hepatocarcinogenesis, although they were poly-morphic between DRH and F rats. INTRODUCTION Chemical-induced hepatocarcinogenesis is a multistep process sub- Two rat strains, Copenhagen (8) and BN (9), have been shown to be resistant to chemical induction of HCC.
Recently, De Miglio et by: Resistance to chemically-induced mammary tumors in Copenhagen X nude-derived F2 athymic rats: evidence that T-cell immunity is not involved in Copenhagen resistance. J E Korkola, G A Wood. In feces from rats living in the sewage system under a Copenhagen hospital researchers have found genes that show resistance towards antibiotics.
Although resistance to antibiotics is expected, of particular concern are the genes showing resistance towards vancomycin – one of the few antibiotics used as a last resort in the treatment of multi resistant bacteria. "Human Polygenic Diseases - Animal Models" deals with the emerging role of complex genetic factors in the pathogenesis of common diseases.
These diseases include hypertension, diabetes, obesity, and cancer, and cause a large fraction of morbidity and death. Complex genetic factors are difficult to study in humans, and this book will give the reader a concise view of the major experimental.
Wood GA, Korkola JE, Archer MC. Resistance of Copenhagen rats to hepatocarcinogenesis does not involve T-cell immunity. Carcinogenesis. Feb;22(2)–9. Korkola JE, Wood GA, Archer MC. Cyclin D1 expression during rat mammary tumor development and its potential role in the resistance of the Copenhagen rat.
rats counterparts [26,27]. The Brown Norway (BN)  and the Copenhagen (Cop) [29,30] rat strains, well-known to be strongly resistant to hepatocellular carcinogenesis, after crossing with F rats, dominantly transmit their resistance to (BNxF)F1 (BFF1) and (CopxF)F1 (CFF1) progeny.
WhenCited by: 1. Expression of the mdr gene also reached high levels in regenerating rat liver 24 to 72 hours after partial hepatectomy. These results show that the expression of the mdr gene can be regulated in liver and is likely to be responsible for part of the multidrug-resistance phenotype of carcinogen-initiated hepatocytes and regenerating liver by: The meeting on experimental hepatocarcinogenesis which took place in Spa, Belgium at the end of May was the Second European Meeting.
About scientists, mostly from Europe but also from the United States, met there for three days in a very friendly atmosphere to exchange knowledge and ideas on experimental and human liver : Springer US.
After 6 months of treatment, neoplastic nodules were observed in 3/8 rats in the DEN-initiated, tamoxifen-treated group. In the initiated group provided with tamoxifen for 15 months, neoplastic nodules were observed in 7/8 rats and hepatocellular carcinomas in 3/8 rats.
The serum level of tamoxifen in these rats was – ng/ by: A rat-race against resistance to antibiotics In feces from rats living in the sewage system under a Copenhagen hospital researchers have found Poster # Title Author(s) 1 Is the Mammary Stroma of Copenhagen Rats a Tumor Suppressor.
Drexler, Schaeberle, Maffini 2 Stromal Influences on the MCF7 Cells Phenotype in 3-Dimensional Cultures Krause, Maffini, Soto, Sonnenschein 3 In Utero Exposure to Bisphenol A: Links with Mammary Gland Cancer Development Murray, Maffini, Sonnenschein, Soto. Title: Mechanisms of Human Hepatocarcinogenesis VOLUME: 3 ISSUE: 6 Author(s):William B.
Coleman Affiliation:Department of Pathology and Laboratory Medicine, Curriculum in Toxicology, UNC Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NCUSA.
Keywords:hepatocarcinogenesis, hepatitis c virus, genetic liver diseases, gene Cited by: Predisposition to hepatocarcinogenesis is under polygenic control.
We analyzed gene expression patterns of dysplastic liver nodules (DN) and hepatocellular carcinoma (HCC) chemically-induced in F and BN rats, respectively susceptible and resistant to hepatocarcinogenesis, to evaluate effector mechanisms of predisposition genes, and commonalties between transcription signatures of rat.
Title:Role of NF-κB in Hepatocarcinogenesis and Its Potential Inhibition by Dietary Antioxidants VOLUME: 12 ISSUE: 9 Author(s):Howard Perry Glauert Affiliation:Graduate Center for Nutritional Sciences, University of Kentucky, Funkhouser Building, Lexington, KYUSA.
Keywords:Antioxidants, carcinogenesis, hepatocellular carcinomas, IκB kinase, NF-κB, vitamin E, Cited by: 4. Workshop: ‘Biomedicine and Aesthetics in a Museum Context’, Copenhagen, August 30 – September 1, The museification of the world (reading Agamben’s Profanations) How can the resistance of museums to the participatory web be explained?.
Examples of alliteration in the book hatchet. How did the Mediterranean climate influence culture in the region. Mice and Rats. Do wood rats move around? We need you to answer this question!Cellular pattern of multidrug-resistance gene expression during chemical hepatocarcinogenesis in the rat (pages –).
Harushige Nakatsukasa, Ritva P. .Is wood rats carnivore? Unanswered Questions. How is the ideal beauty exemplified in aphrodite of melos. Look at this painting this painting was created by what type of artist.