ライフサイエンスコーパス: MEN1 gene

1 centromeric and telomeric boundaries for the MEN1 gene.

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

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

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

5 ine pancreas, due to the inactivation of 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 lting from loss-of-function mutations in the MEN1 gene.

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

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

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

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

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

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

15 quential inactivation of both alleles of the MEN1 gene.

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

17 ttempt to further define the location of 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 Mutations in the MEN1 gene are broadly distributed throughout its nine pr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 the MEN1 syndrome, in which mutations in the MEN1 gene lead to loss or inactivation of MENIN protein.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 MEN1 gene mutations were found to be exclusively enriche

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 omatin adapter protein menin, encoded by the MEN1 gene, to sustain aberrant leukaemogenic gene expres

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

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

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

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

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

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

96 The MEN1 gene was recently isolated by positional cloning.

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

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

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

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

101 11 (36%) sporadic tumors, both copies of the MEN1 gene were inactivated.

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

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

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

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

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