Zobrazeno 1 - 10
of 35
pro vyhledávání: '"W F, Dove"'
Publikováno v:
The Journal of Cell Biology
Scopus-Elsevier
Scopus-Elsevier
Min is a fully penetrant dominant mutation that leads to the development of multiple intestinal adenomas throughout the duodenal-to-colonic axis. Min/+ C57BL6/J mice have an average life-span of 120 d. Multi-label immunocytochemical studies of these
Autor:
R T, Cormier, W F, Dove
Publikováno v:
Cancer research. 60(14)
Altered patterns of the 5-cytosine methylation of genomic DNA are associated with the development of a wide range of human cancers. We have studied the mechanisms and genetic pathways by which a targeted heterozygous deficiency in the murine 5-cytosi
Publikováno v:
Cancer research. 57(10)
We have demonstrated previously that intestinal tumor formation in B6 Min/+ mice is always accompanied by loss of the wild-type adenomatous polyoposis coli (Apc) allele and that intestinal tumor multiplicity in B6 Min/+ mice can be significantly incr
Publikováno v:
Biochimica et biophysica acta. 1332(2)
Autor:
W F, Dove, L, Clipson, K A, Gould, C, Luongo, D J, Marshall, A R, Moser, M A, Newton, R F, Jacoby
Publikováno v:
Cancer research. 57(5)
We have tested the hypothesis that enteric bacteria are necessary for formation of intestinal adenomas in C57BL/6-ApcMin/+ mouse. Germ-free mice developed 2-fold fewer adenomas than conventional controls in the medial small intestine (7.3 versus 14.9
Publikováno v:
Genes, chromosomescancer. 17(3)
We have found previously that all spontaneous intestinal adenomas from Apc+/ApcMin mice lose the wild type Apc marker on two genetic backgrounds. On the (AKR x B6)F1 background, this event involves loss of the entire homolog of mouse chromosome 18 ca
Autor:
K A, Gould, W F, Dove
Publikováno v:
Cell growthdifferentiation : the molecular biology journal of the American Association for Cancer Research. 7(10)
Mice heterozygous for Min, a mutant allele of Apc, develop adenomas throughout the intestinal tract. Tumor multiplicity in Min mice is influenced by genetic modifier loci. Previously, we mapped one of these modifier loci, Mom1, to distal mouse chromo
Autor:
Y, Beazer-Barclay, D B, Levy, A R, Moser, W F, Dove, S R, Hamilton, B, Vogelstein, K W, Kinzler
Publikováno v:
Carcinogenesis. 17(8)
The Min mouse provides a genetically defined model for inherited and sporadic forms of human colorectal tumorigenesis. To test the suitability of this model for the evaluation and optimization of chemopreventive agents, we examined the effects of sul
Autor:
R F, Jacoby, D J, Marshall, M A, Newton, K, Novakovic, K, Tutsch, C E, Cole, R A, Lubet, G J, Kelloff, A, Verma, A R, Moser, W F, Dove
Publikováno v:
Cancer research. 56(4)
C57BL/6J-Min/+mice (n = 56), heterozygous for a nonsense mutation in the Apc gene, were randomized at weaning to seven groups, including groups treated with piroxicam at 0, 50, 100, and 200 ppm in the AIN93G diet. After only 6 weeks of treatment, int
Publikováno v:
Cancer research. 55(19)
The timing of intestinal tumor initiation in B6-Min/+ mice has been examined by treating mice at 5-35 days of age with a single i.p. injection of the direct-acting alkylating agent N-ethyl-N-nitrosourea (ENU). Treatment of Min/+ mice at 5-14 days of