ライフサイエンスコーパス: MEN1 gene

1 ill be valuable tools for the cloning of the MEN1 gene.

2 many months after loss of both copies of the Men1 gene.

3 ecombinase, resulting in the deletion of the Men1 gene.

4 ine pancreas, due to the inactivation of the MEN1 gene.

5 lting from loss-of-function mutations in the MEN1 gene.

6 and caused by inactivating mutations in the MEN1 gene.

7 these tumors have focused on the role of the MEN1 gene.

8 m patients with MEN1 for allelic loss of the MEN1 gene.

9 he consequence of a germline mutation in the MEN1 gene.

10 nd one lipoma showed allelic deletion of the MEN1 gene.

11 t sporadic MEN1) were distributed across the MEN1 gene.

12 ic markers spanning the area of the putative MEN1 gene.

13 NP36 gene was studied as a candidate for the MEN1 gene.

14 quential inactivation of both alleles of the MEN1 gene.

15 b of D11S913, a marker tightly linked to the MEN1 gene.

16 ttempt to further define the location of the MEN1 gene.

17 centromeric and telomeric boundaries for the MEN1 gene.

18 enes have already been excluded as candidate MEN1 genes.

19 as at multiple sites are monoclonal and that MEN1 gene alterations in gastrinomas occur before the de

20 and some mesenchymal tumors have documented MEN1 gene alterations on chromosome 11q13.

21 arise as independent clones, develop through MEN1 gene alterations, and are an integral part of MEN1.

22 We recently cloned the MEN1 gene and confirmed its identity by finding mutation

23 age, >80% of mice homozygous for the floxed Men1 gene and expressing RIP-cre develop multiple pancre

24 We recently cloned the MEN1 gene and identified MEN1 germline mutations in four

25 denomas showed a deletion of one copy of the MEN1 gene, and a specific MEN1 gene mutation in the rema

26 G), and multiple endocrine neoplasia type-1 (MEN1) genes, and of MINT1, MINT2, MINT25, MINT27 and MIN

27 Mutations in the MEN1 gene are associated with the multiple endocrine neo

28 o determine whether somatic mutations in the MEN1 gene are present.

29 of 10 different siRNAs corresponding to the MEN1 gene by examining the expression of two additional

30 The MEN1 gene called MENIN maps to chromosome 11q13 and is t

31 The MEN1 gene causing MEN1 is a tumor suppressor gene and se

32 The MEN1 gene contains 10 exons and encodes a ubiquitously e

33 d tumor) showed allelic loss that placed the MEN1 gene distal to marker PYGM.

34 The MEN1 gene encodes the tumor suppressor menin of 610 amin

35 This syndrome results from mutations in the MEN1 gene, encoding menin.

36 We introduced a Men1 gene flanked by loxP sites into the mouse germ line

37 had biological effects, directly supporting MEN1 gene function as a tumor suppressor.

38 Here, we show that loss of Men1 gene function in the parathyroid glands of mice res

39 hyroidism resulting from the deletion of the Men1 gene in parathyroid tissue.

40 cidate the potential etiological role of the MEN1 gene in pituitary tumorigenesis, 39 sporadic pituit

41 To elucidate the etiological role of the MEN1 gene in sporadic enteropancreatic endocrine tumorig

42 The data implicate the MEN1 gene in the pathogenesis of sporadic lung carcinoid

43 lopment of these tumors or mechanisms of the MEN1 gene inactivation that do not involve large deletio

44 A alterations, including disparate roles for MEN1 gene inactivation, indicate that markedly different

45 gressively narrows the size of the candidate MEN1 gene interval on the chromosome and then finds and

46 on studies in enteropancreatic ETs suggested MEN1 gene involvement in tumorigenesis of familial pancr

47 To test whether the MEN1 gene is involved in the pathogenesis of multiple sm

48 The present data indicate the MEN1 gene is located between markers D11S1883 and D11S49

49 The isolation of the MEN1 gene is necessary to further define its role in pat

50 However, the MEN1 gene is not a significant contributor to the tumori

51 o acid residues, menin, and mutations in the Men1 gene lead to the MEN1 syndrome.

52 ere, we show that targeted disruption of the Men1 gene leads to enhanced cell proliferation, whereas

53 together, the present data suggest that the MEN1 gene lies between PYGM and D11S4936, a region of ap

54 In contrast, LOH at the MEN1 gene locus was demonstrated only in 2 of 40 (5%) sp

55 ed using four polymorphic DNA markers at the MEN1 gene locus; D11S480, PYGM, D11S449, and INT-2.

56 erozygous disruption of the tumor suppressor Men1 gene (Men1(+/-)) develop tumors in the pituitary, p

57 nin tumor suppressor protein, product of the MEN1 gene mutated in familial multiple endocrine neoplas

58 hods was used to assess clonality, including MEN1 gene mutation analysis, loss of heterozygosity anal

59 All four tumors showed the presence of a MEN1 gene mutation and loss of the other allele.

60 Thus, somatic MEN1 gene mutation contributes to tumorigenesis in a sub

61 Thus, somatic MEN1 gene mutation for the mutant allele.

62 Among 33 tumours we found somatic MEN1 gene mutation in 7, while the corresponding MEN1 ge

63 of one copy of the MEN1 gene, and a specific MEN1 gene mutation in the remaining gene copy was detect

64 even tumors showed neither the presence of a MEN1 gene mutation nor 11q13 LOH.

65 All tumours with MEN1 gene mutation showed LOH on 11q13, making the tumou

66 In three patients, a somantic MEN1 gene mutation was detected in the tumor.

67 H at chromosome 11q13 and a complex germline MEN1 gene mutation.

68 om a familial MEN1 patient were examined for MEN1 gene mutations and allelic deletions.

69 mas and 12 insulinomas) from 40 patients for MEN1 gene mutations and allelic deletions.

70 The data suggest that somatic MEN1 gene mutations and deletions play a causative role

71 Somatic MEN1 gene mutations and deletions play a critical role i

72 MEN1 gene mutations were identified in 9 of 27 (33%) spo

73 The MEN1 gene, mutations in which are responsible for multip

74 or suppressor gene loci, one on 3p25 and the MEN1 gene on 11q13, have thus far been implicated in the

75 lways have loss-of-function mutations in the MEN1 gene on chromosome 11, and endocrine tumors arising

76 of heterozygosity (LOH) at the locus of the MEN1 gene on chromosome 11q13, and for mutations of the

77 sporadic endocrine tumors independent of the MEN1 gene or in other tumors, such as breast cancer, tha

78 The present results suggest that the MEN1 gene plays a role in all four tumor types.

79 Besides its endocrine role, the Men1 gene product menin interacts with the mixed lineage

80 ggest that loss of function of the wild-type MEN1 gene product plays a role in the development of ang

81 Our findings establish that MEN1 gene replacement therapy can generate menin express

82 Genetic alterations of the MEN1 gene represent a candidate pathogenetic mechanism o

83 Mutations in the MEN1 gene that encodes for the menin protein are the pre

84 ndrome that results from the mutation of the MEN1 gene that encodes protein menin.

85 dy, we conducted a preclinical evaluation of MEN1 gene therapy in pituitary tumors of Men1(+/-) mice,

86 n chromosome 11q13, and for mutations of the MEN1 gene using dideoxy fingerprinting.

87 llelic deletion of the remaining copy of the MEN1 gene was also found in the patient's tumor.

88 The MEN1 gene was finally identified because it was the one

89 One copy of the MEN1 gene was found to be deleted in 25 of 27 (93%) spor

90 During the course of cloning SIPA-1, the MEN1 gene was identified, thus excluding human SIPA-1 as

91 dy, the centromeric boundary of the putative MEN1 gene was PYGM.

92 The MEN1 gene was recently isolated by positional cloning.

93 In addition, the MEN1 gene was the gene most likely to show acquired muta

94 As a step toward cloning the MEN1 gene, we have constructed a 2.8-Mb clone contig con

95 ological consequences of the deletion of the MEN1 gene, we set out to create a mouse model of hyperpa

96 ures of gastrinomas; deletions involving the MEN1 gene were con firmed, but the rest of the genome wa

97 11 (36%) sporadic tumors, both copies of the MEN1 gene were inactivated.

98 Whereas deletions encompassing the MEN1 gene were seen in two tumors, the most striking res

99 ial tumor syndrome linked to mutation of the MEN1 gene, which encodes a tumor suppressor, menin.

100 This syndrome results from mutations in the MEN1 gene, which encodes menin protein.

101 te and temporally controlled excision of the Men1 gene, which encodes menin, ameliorated preexisting

102 e 11q13, and linkage analysis has placed the MEN1 gene within a 2-Mb interval flanked by D11S1883 and