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1 MEN2A is a dominantly-inherited cancer predisposition sy
2 s with multiple endocrine neoplasia type 2A (MEN2A) and familial medullary thyroid carcinoma (FMTC) c
4 drive multiple endocrine neoplasia type 2A (MEN2A), a hereditary syndrome associated with the develo
7 that induction of the constitutively active MEN2A-specific RET mutant, RET2A(C634R), correlates with
8 protein previously associated with FMTC and MEN2A, it is very likely that they represent mutations t
9 rranged during Transfection (RET) gene cause MEN2A, MEN2B, and familial medullary thyroid carcinoma (
10 We have developed a Drosophila model for MEN2A and MEN2B diseases by targeting oncogenic forms of
11 d by germline mutations in the RET (formerly MEN2A, MEN2B) proto-oncogene located on chromosomal band
12 to construct mice in which the most frequent MEN2A mutation, Cys-634-Arg, was expressed under the con
14 between G691S/S904S and modifier effects in MEN2A families in any of the four European families anal
16 tential key mechanism of cancer induction in MEN2A, both in the absence and presence of its native li
18 a cysteine replacement that is prevalent in MEN2A cases - the A639G/A641R mutations significantly re
19 ns of RET lead to other conditions including MEN2A, familial medullary thyroid carcinoma and intestin
20 C) and type 2A multiple endocrine neoplasia (MEN2A), mutations of cysteine residues in the extracellu
21 ing the cysteine-rich region of the protein (MEN2A-like mutations) are correlated with different phen
28 re significantly deregulated in tumours with MEN2A-like and MEN2B-like mutations; however, further in
29 ositive weak effect on tumor spectrum within MEN2A, which requires replication in a larger series.