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1 ted activation of a proangiogenic program in intestinal polyps.
2 ected thyroid and adrenal medulla tumors and intestinal polyps.
3 oss of p85beta led to increased incidence of intestinal polyps.
4 were also associated with greater numbers of intestinal polyps.
5 C-mutated human colon cancers and Apc(min/+) intestinal polyps.
6 gnificant increase in the number and size of intestinal polyps.
7 were 110 or 200 days of age and screened for intestinal polyps.
8 , the presumptive precursor lesions to gross intestinal polyps.
10 e STK11/LKB1 gene, sequencing analysis of an intestinal polyp and pancreatic cancer from this patient
11 on of enzyme inhibition has shown synergy in intestinal polyp and tumor models, the exact mechanism f
12 cient background showed a 4-fold increase in intestinal polyps and a 2-fold increase in colonic tumor
13 f prostate neoplasia, endometrial carcinoma, intestinal polyps and adrenal lesions in Pten(+/-) mice.
14 r prevention and/or therapeutic treatment of intestinal polyps and cancers by oral administration of
17 dominant disorder characterized by multiple intestinal polyps and, without surgical intervention, th
18 gous for germ line Cdx2 inactivation develop intestinal polyps, and the lesions lack Cdx2 expression.
19 This may be because these mice have a higher intestinal polyp burden as a result of the enhancement o
20 ressed the colon polyps completely and small intestinal polyps by >86% (P < 0.0001) compared with the
21 celecoxib decreased the rate of formation of intestinal polyps by approximately 70% (P < 0.0001).
22 bcapsular hepatic veins, enlarged glomeruli, intestinal polyps containing endothelial cell masses, ab
23 n of Zfp148 in a mouse model of Apc-mediated intestinal polyps demonstrated that ZBP-89 was required
24 eas: (i) intestinal polyp multiplicity, (ii) intestinal polyp distribution, and (iii) extraintestinal
25 noma-carcinoma sequence, it is proposed that intestinal polyps evolve through a set of defined mutati
26 ut of Dnmt1 and could substantially suppress intestinal polyp formation when applied to an ApcMin mod
27 tion, CP-31398 also significantly suppressed intestinal polyp formation, albeit to a lesser extent th
31 Here we show that Lkb1(+/-) mice develop intestinal polyps identical to those seen in individuals
32 reported that it could inhibit the growth of intestinal polyp in animals and in patients with the fam
33 th of LLC tumors, the number and the size of intestinal polyps in Apc(Min) (/+) mice, thus strongly i
34 nt reduction in the number and size of small intestinal polyps in APC(min+/-) mice treated with eithe
37 y factor in the formation of multiple benign intestinal polyps in PJS patients, and possibly for the
38 to evaluate its effects on the formation of intestinal polyps in the Min/+ mouse model for colorecta
39 homologous recombination developed multiple intestinal polyp-like lesions that did not express Cdx2
40 ied modifiers in the C3H strain can suppress intestinal polyp multiplicity in Apc(Min/+) mice, and ac
41 their reported variation in three areas: (i) intestinal polyp multiplicity, (ii) intestinal polyp dis
42 a2) background results in a 90% reduction in intestinal polyp number relative to Apc(Min) mice carryi
43 om1 locus on the B6 background reduced small intestinal polyp numbers by 50% and colon polyp incidenc
44 ) locus on the C3H background, reduced small intestinal polyp numbers by 80% and colon polyp incidenc
45 he protein is significantly increased in the intestinal polyps of ApcMin/+ mice has led us to hypothe
47 a statistically significant increase in both intestinal polyp size and number when compared with BAH
48 c treatment induce apoptosis specifically in intestinal polyps, strongly inhibit tumour growth, and p
49 ) gene, dramatically increases the number of intestinal polyps that develop in the multiple intestina
52 ensin homolog (PTEN) generates hamartomatous intestinal polyps with epithelial and stromal involvemen
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