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1 essfully treated by surgical excision of the microadenoma.
2  Brain magnetic resonance showed a pituitary microadenoma.
3 l-death activation, as well as generation of microadenomas.
4 48.2% of the total cohort were found to have microadenomas.
5 e cells, and formation of ectopic crypts and microadenomas.
6 pha-cell hyperplasia and glucagon-expressing microadenomas (3 of 8) and a neuroendocrine tumor.
7            Hyperplastic ACF, dysplastic ACF, microadenomas, adjacent normal-appearing epithelium, and
8                       Remaining adenomas and microadenomas almost exclusively contained the non-recom
9 cell dysplasia at birth, which progresses to microadenomas and acinar cell carcinomas.
10 OR pathway by rapamycin reduced formation of microadenomas and polyps in the Apcmin/+/Sigirr-/- mice.
11 s coli (Apc)min/+/Sigirr-/- mice for polyps, microadenomas, and anaphase bridge index.
12          In 47 centers (18.8%), GH-secreting microadenomas are often treated pharmacologically first.
13 ion is variable for each type of tumor, with microadenomas being either silent or manifesting with sy
14              Moreover, a few stratified foci/microadenomas containing hyperproliferative cells, resem
15  assessment are warranted for macroadenomas, microadenomas, cystic lesions and empty sella, as well a
16 e for Dnmt3b in the transition stage between microadenoma formation and macroscopic colonic tumor gro
17  increased loss of heterozygosity of Apc and microadenoma formation, resulting in spontaneous colonic
18 ate that the loss of Dnmt3b has no impact on microadenoma formation, which is considered the earliest
19 s and increased epithelial proliferation and microadenoma formation.
20  foci and decreased the incidence of colonic microadenomas from 75% to 33% (P<0.05).
21 enotype of macroadenomas and laser dissected microadenomas, global and regional DNA methylation and g
22        Mutation of both Apc and Kras yielded microadenomas in both the cecum and the proximal colon,
23 dence of visible colon tumors and dysplastic microadenomas in ER-deficient Min/+ relative to Er(+/+)M
24 e formation of spontaneous macroadenomas and microadenomas in the distal small intestine and colon of
25  occurs in two stages, with the formation of microadenomas leading to the development of macroscopic
26 r macroadenomas (>=10 mm) (48% of tumors) or microadenomas (&lt;10 mm).
27                        Approximately 50% are microadenomas (&lt;10 mm); the remainder are macroadenomas
28 sulting in an approximately 50% reduction of microadenoma numbers and significantly reduced average a
29 were altered in apparently normal crypts and microadenomas of mice carrying germline Apc mutations, s
30 e) caused a twofold increase in apoptosis in microadenomas, resulting in an approximately 50% reducti
31 noid biosynthetic enzyme cyclooxygenase-2 in microadenomas, suggesting that these regulators are key
32 thylation, we observed elevated incidence of microadenomas that were associated with LOH at Apc.
33 als revealed no differences in the number of microadenomas, the presumptive precursor lesions to gros
34  were clonal, but at least 76 percent of the microadenomas were polyclonal in origin.
35                          Gross tumors and/or microadenomas were then evaluated.
36 ld and increased the average size of colonic microadenomas, whereas Dnmt3a1 had no effect.
37              The cure rate for patients with microadenomas who had no previous therapy was 90% (123 o