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1 posing the neoplastic progression of colonic aberrant crypt foci.
2 methane (AOM)-induced preneoplastic lesions, aberrant crypt foci.
3 mas, and in even earlier microscopic colonic aberrant crypt foci.
4 dUrd incorporation, and in the appearance of aberrant crypt foci.
5 ed the formation of very early, precancerous aberrant crypt foci.
6 ssion was observed in preneoplastic lesions (aberrant crypt foci, 3.7-fold) compared with saline-trea
7 inctly higher expression was found in 4 of 7 aberrant crypt foci, 32 of 36 adenomas, 18 of 28 primary
8 bined with celecoxib on azoxymethane-induced aberrant crypt foci (ACF) and colon adenocarcinomas in F
9 s showed that the number of aberrant crypts, aberrant crypt foci (ACF) and crypts/focus in rats of th
10 empt to demonstrate the relationship between aberrant crypt foci (ACF) and subsequent colonic neoplas
11  the formation of chemically induced colonic aberrant crypt foci (ACF) and tumors, cyclooxygenase (CO
12                                              Aberrant crypt foci (ACF) are collections of abnormal co
13                                              Aberrant crypt foci (ACF) are distinct microscopic lesio
14                                              Aberrant crypt foci (ACF) are grossly invisible putative
15                                              Aberrant crypt foci (ACF) are morphologically abnormal s
16                                              Aberrant crypt foci (ACF) are postulated to be the earli
17                                              Aberrant crypt foci (ACF) are postulated to be the earli
18                                              Aberrant crypt foci (ACF) are putative precursors of at
19                                              Aberrant crypt foci (ACF) are the earliest identified ne
20 nd study, using azoxymethane-induced colonic aberrant crypt foci (ACF) as a measure of efficacy.
21 molecular studies, which support the role of aberrant crypt foci (ACF) as a putative precursor to col
22 mice subjected to AOM had significantly less aberrant crypt foci (ACF) formation and significantly re
23  BER deficiency would interact to accelerate aberrant crypt foci (ACF) formation and tumor developmen
24 th AOM showed a 60% increase in premalignant aberrant crypt foci (ACF) formation over LOI(-) mice.
25       We examined the colonic microbiota and aberrant crypt foci (ACF) in C57BL/6N female mice fed va
26 y examining regression of chemically induced aberrant crypt foci (ACF) in the colon of CF1 mice and i
27 ir ability to inhibit the formation of colon aberrant crypt foci (ACF) induced by a s.c. injection of
28 nation of both as there was no difference in aberrant crypt foci (ACF) or tumor burden when animals w
29 develop putative premalignant lesions called aberrant crypt foci (ACF) that are localized to the dist
30                               Sections of 70 aberrant crypt foci (ACF), 55 adenomas, 84 primary color
31 n this basis, we predicted that hyperplastic aberrant crypt foci (ACF), a putative precancerous lesio
32 s against azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF), against AOM and dextran sulfa
33  histopathological features of preneoplastic aberrant crypt foci (ACF), gene expression analysis was
34                                              Aberrant crypt foci (ACF), the earliest identified neopl
35 ribe the expression of beta-catenin in human aberrant crypt foci (ACF), the earliest identified neopl
36 -associated DNA methylation changes in human aberrant crypt foci (ACF), the earliest putative precurs
37 reduced the size and number of preneoplastic aberrant crypt foci (ACF).
38 ysis, with a subset undergoing assessment of aberrant crypt foci (ACF).
39 r, on the development of AOM-induced colonic aberrant crypt foci (ACF).
40 in the colon and in the formation of colonic aberrant crypt foci (ACF).
41 elopment, we compared DNA fingerprints of 44 aberrant crypt foci (ACF; the earliest identified neopla
42                                              Aberrant crypt foci (ACFs) were similarly increased sign
43                 Histological sections of the aberrant crypt foci and adjacent mucosa were evaluated f
44 t further evidence of a relationship between aberrant crypt foci and colon cancer in humans.
45        There is a strong association between aberrant crypt foci and colon cancer, including many sha
46 on with dextran sodium sulfate; formation of aberrant crypt foci and colon tumors was examined.
47 so significantly reduced the number of large aberrant crypt foci and decreased the incidence of colon
48 betaII) expression was slightly decreased in aberrant crypt foci and dramatically reduced in colon tu
49 reated animals exhibited significantly fewer aberrant crypt foci and increased apoptotic activity in
50 tation (orthologous to human APC(1309)) have aberrant crypt foci and low- and high-grade dysplastic a
51           NAG-(Tg+) mice developed 50% fewer aberrant crypt foci and no tumors, in comparison with no
52 /- mice developed fewer azoxymethane-induced aberrant crypt foci and tumors.
53 ese data lend support to the hypothesis that aberrant crypt foci are precursors of some colon cancers
54                                              Aberrant crypt foci are putative preneoplastic lesions f
55  cyclin D1 expression throughout microscopic aberrant crypt foci arising in 15-PGDH null colons and i
56 P1 immunostaining was observed in dysplastic aberrant crypt foci as well as in small adenomas.
57 ce developed increased (P < 0.05) numbers of aberrant crypt foci at 8 weeks.
58 er, there was no difference in the number of aberrant crypt foci between these groups, and thus the e
59   The multiplicity of macroscopic tumors and aberrant crypt foci both increased by ~50% in the hybrid
60 he effect of dietary Cer-beta-glucuronide on aberrant crypt foci correlated significantly with the le
61 al or in vitro studies include cytokinetics, aberrant crypt foci, eicosanoids and hydroxyoctadecadien
62 pressing mice resulted in markedly decreased aberrant crypt foci formation and substantially reduced
63 specific COX-2 inhibitor, suppressed colonic aberrant crypt foci formation induced by azoxymethane in
64 esulted in a reduction in carcinogen-induced aberrant crypt foci formation.
65                                     Multiple aberrant crypt foci from a single patient were identifie
66 catenin expression levels, and the number of aberrant crypt foci in the colon endothelium.
67 ors could not be explained by differences in aberrant crypt foci number.
68      These changes preceded the formation of aberrant crypt foci or adenoma.
69  carcinogenesis, the total number of colonic aberrant crypt foci per animal (control, 161 +/- 11) and
70 eased susceptibility to azoxymethane-induced aberrant crypt foci, preneoplastic lesions in the colon.
71 tion (DNA adduct formation) and promotional (aberrant crypt foci) stages.
72 a of the intestinal mucosa and production of aberrant crypt foci, suggesting a novel role of DNA-PKcs
73 ely overexpressed in colorectal cancer, from aberrant crypt foci to advanced carcinomas.
74                              The size of the aberrant crypt foci was larger in the colon than in the
75 n in the cecum, and the highest frequency of aberrant crypt foci was observed in the cecum.
76                             The frequency of aberrant crypt foci was significantly higher (2-3-fold)
77  weeks of treatment, intestinal adenomas and aberrant crypt foci were counted, and serum levels of pi
78 t with sporadic colon cancer identified with aberrant crypt foci with carcinoma in situ is described.
79                                              Aberrant crypt foci with dysplasia are thought to be the

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