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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 e cells, and formation of ectopic crypts and microadenomas.
9 OR pathway by rapamycin reduced formation of microadenomas and polyps in the Apcmin/+/Sigirr-/- mice.
11 ion is variable for each type of tumor, with microadenomas being either silent or manifesting with sy
13 e for Dnmt3b in the transition stage between microadenoma formation and macroscopic colonic tumor gro
14 increased loss of heterozygosity of Apc and microadenoma formation, resulting in spontaneous colonic
15 ate that the loss of Dnmt3b has no impact on microadenoma formation, which is considered the earliest
18 enotype of macroadenomas and laser dissected microadenomas, global and regional DNA methylation and g
20 dence of visible colon tumors and dysplastic microadenomas in ER-deficient Min/+ relative to Er(+/+)M
21 e formation of spontaneous macroadenomas and microadenomas in the distal small intestine and colon of
22 occurs in two stages, with the formation of microadenomas leading to the development of macroscopic
24 sulting in an approximately 50% reduction of microadenoma numbers and significantly reduced average a
25 were altered in apparently normal crypts and microadenomas of mice carrying germline Apc mutations, s
26 e) caused a twofold increase in apoptosis in microadenomas, resulting in an approximately 50% reducti
27 noid biosynthetic enzyme cyclooxygenase-2 in microadenomas, suggesting that these regulators are key
29 als revealed no differences in the number of microadenomas, the presumptive precursor lesions to gros
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