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1 MEN1, the tumor suppressor gene disrupted in multiple endocrine neoplasia type 1.
2 , as compared with none of the patients with multiple endocrine neoplasia type 1.
3 n the diverse nature of the benign tumors in multiple endocrine neoplasia type 1.
4 -Ellison syndrome or nonfunctional PETs with multiple endocrine neoplasia-type 1.
6 missense mutations found in individuals with multiple endocrine neoplasia type 1, and the interacting
7 in patients with ZES, especially those with multiple endocrine neoplasia type 1, and the precise ord
8 uitary neoplasias: McCune-Albright syndrome, multiple endocrine neoplasia type 1, Carney complex and,
9 ith lymph node involvement and patients with multiple endocrine neoplasia type 1 did not demonstrate
11 product of the MEN1 gene mutated in familial multiple endocrine neoplasia type 1, has not been define
12 ar, the areas of gastrinoma, insulinoma, and multiple endocrine neoplasia type 1 have received carefu
13 from pituitary adenomas in two patients with multiple endocrine neoplasia type 1 in which cells with
17 ect genetic evidence that MEN1, the gene for multiple endocrine neoplasia type 1, is a tumor suppress
18 ncing analysis, and deletion analysis of the multiple endocrine neoplasia type 1 locus succeeded in t
19 g in a large group of extended families with multiple endocrine neoplasia type 1 (MEN 1), with the ul
20 nts with sporadic ZES, but not in those with multiple endocrine neoplasia type 1 (MEN-1) and ZES, the
21 of heterozygosity (LOH) at the locus of the multiple endocrine neoplasia type 1 (MEN-1) gene was stu
24 S were studied prospectively, with 39 having multiple endocrine neoplasia, type 1 (MEN-1) (high incre
26 previously identified at the locus linked to multiple endocrine neoplasia type 1 (MEN1) and as prespl
43 s occur both sporadically and as part of the multiple endocrine neoplasia type 1 (MEN1) syndrome.
44 nscriptionally active chromatin, whereas the multiple endocrine neoplasia type 1 (MEN1) tumor suppres
48 they are especially common in patients with multiple endocrine neoplasia type 1 (MEN1), and most stu
49 gene, mutations in which are responsible for multiple endocrine neoplasia type 1 (MEN1), encodes a 61
51 crine tumor susceptibility syndromes such as multiple endocrine neoplasia type 1 (MEN1), von Hippel L
61 beta), T-type calcium channel (CACNA1G), and multiple endocrine neoplasia type-1 (MEN1) genes, and of
62 have shown that the gene responsible for the multiple endocrine neoplasia type-1 (MEN1) syndrome loca
66 sm (FIHP), or as part of a syndrome, such as multiple endocrine neoplasia type 1 or hyperparathyroidi
67 e Zollinger-Ellison syndrome who do not have multiple endocrine neoplasia type 1 or metastatic diseas
72 nts, 123 had sporadic gastrinomas and 28 had multiple endocrine neoplasia type 1 with an imaged tumor
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