ライフサイエンスコーパス: gastrinoma

1 e surgical techniques to localize and remove gastrinoma.

2 th neurofibromatosis type 2 and a pancreatic gastrinoma.

3 orphologic features suggestive of pancreatic gastrinoma.

4 , colocalized with gastrin in human duodenal gastrinomas.

5 pancreatic ETs (nongastrinomas) and sporadic gastrinomas.

6 it be the imaging modality in patients with gastrinomas.

7 adic insulinomas, and 8 of 18 (44%) sporadic gastrinomas.

8 e initial imaging modality for patients with gastrinomas.

9 gery (P = 0.004), but it still missed 20% of gastrinomas.

10 trinomas and 5 patients (19%) had pancreatic gastrinomas.

11 e rate due to the detection of more duodenal gastrinomas.

12 this is the first report of such a defect in gastrinomas.

13 screen for bone metastases in patients with gastrinomas.

14 for localizing neuroendocrine tumors such as gastrinomas.

15 re strikingly different from the LOH rate of gastrinomas (21%), suggesting that the mechanism that dr

16 gastrinomas), 14 of 34 (41%) MEN1-associated gastrinomas, 3 of 16 (19%) sporadic insulinomas, and 8 o

17 Among the patients with sporadic gastrinomas, 34 percent were free of disease at 10 years

18 Twelve gastrinomas (44%) had Chr 1 LOH, and in all of the cases

19 a pancreatic PET, 53% and 68% had a duodenal gastrinoma, 65% and 71% had lymph node metastases, and 0

20 A specific MEN1 mutation was detected in one gastrinoma and in the corresponding germ-line DNA of a p

21 In the present study, 12 gastrinoma and nonfunctioning pancreatic neuroendocrine

22 Two tumors (one gastrinoma and one parathyroid tumor) showed an LOH boun

23 mproved understanding of the pathogenesis of gastrinoma and pancreatic neuroendocrine tumors, new pro

24 ES underwent resection of a primary duodenal gastrinoma and regional nodal metastases with curative i

25 growth rate of untreated hepatic metastatic gastrinoma and to identify its predictors.

26 ocrine tumorigenesis, we analyzed tumors (28 gastrinomas and 12 insulinomas) from 40 patients for MEN

27 ns were identified in 9 of 27 (33%) sporadic gastrinomas and 2 of 12 (17%) insulinomas and were not s

28 Of these patients, 123 had sporadic gastrinomas and 28 had multiple endocrine neoplasia type

29 atients with gastrinoma in MEN1 had duodenal gastrinomas and 5 patients (19%) had pancreatic gastrino

30 ata suggest that 1q LOH is not infrequent in gastrinomas and could be a molecular/genetic prognostic

31 und to be deleted in 25 of 27 (93%) sporadic gastrinomas and in 6 of 12 (50%) sporadic insulinomas.

32 Gastrinomas and insulinomas are frequent in multiple end

33 udy we determine whether Chr 1 LOH occurs in gastrinomas and is associated with aggressive growth by

34 itical role in the tumorigenesis of sporadic gastrinomas and may also contribute to the development o

35 in an increasing proportion of patients with gastrinomas and related neuroendocrine functional tumors

36 of 11q13 LOH in MEN1-associated and sporadic gastrinomas and sporadic insulinomas as compared to MEN1

37 However, only a few MEN1-associated duodenal gastrinomas and sporadic pancreatic nongastrinomas have

38 in microdissected tumor tissue from 27 human gastrinomas and the leukocyte DNA of the patients.

39 Four tumors (two parathyroid tumors, one gastrinoma, and one lung carcinoid tumor) showed allelic

40 ompared with 100 cases of sporadic abdominal gastrinomas, and the evidence reviewed suggests why ZES

41 At presentation, up to 25% of gastrinomas are metastasized, predominantly to the liver

42 Gastrinomas are neuroendocrine neoplasms that occur spor

43 SRS will alter the disease-free rate, which gastrinomas are not detected, what factors contribute to

44 Primary duodenal gastrinomas are now recognized as a common etiology for

45 graphy should be undertaken because duodenal gastrinomas are often minute and multicentric.

46 Gastrinomas are rare functional neuroendocrine tumors ca

47 Gastrinomas are rare gastrin-secreting endocrine tumors

48 clinical course of unselected patients with gastrinomas as well as other functional pancreatic endoc

49 a role in the molecular pathogenesis of most gastrinomas, as suggested in a previous study involving

50 We conclude that sporadic gastrinomas at multiple sites are monoclonal and that ME

51 shown to increase the detection of duodenal gastrinomas, but it is unknown if it alters rate of cure

52 If a primary gastrinoma cannot be identified by SRS or STIR-MRI, endo

53 Other tumors, including gastrinoma, carcinoid, adrenal cortical tumors, angiofib

54 The existence of lymph node (LN) primary gastrinoma causing ZES is controversial.

55 se report describes a patient with a cardiac gastrinoma causing Zollinger-Ellison syndrome.

56 cardiac tumor, the other known locations of gastrinomas causing ZES, was found on detailed tumor ima

57 equently cause neuroendocrine tumors such as gastrinomas, characterized by their predominant duodenal

58 Insulinomas and gastrinomas comprise the majority of functional pancreat

59 match repair defects as importan features of gastrinomas; deletions involving the MEN1 gene were con

60 A proportion of gastrinomas demonstrates aggressive growth, and most dea

61 rwent either distal pancreatic resections or gastrinoma enucleation with lymphadenectomy, 2 patients

62 ture, more sensitive methods to detect small gastrinomas, especially in the duodenum and in periduode

63 fication and expression was determined in 43 gastrinomas from different patients.

64 tudy was to analyze clonality in 20 sporadic gastrinomas from eight patients in whom the tumor was pr

65 l carcinoma of the thyroid, and 1 each had a gastrinoma, glucagonoma, fibrolamellar cancer, and malig

66 In ZES, gastrinoma growth is now the main single determinant of

67 Nevertheless, gastrinomas have become a paradigm for the study of horm

68 In MEN1, multiple gastrinomas have been shown to arise by independent clon

69 An experienced surgeon can find gastrinoma in almost every patient (98%) and nearly one

70 The exact identification of this gastrinoma in an extra-abdominal site was facilitated by

71 Twenty-two (81%) patients with gastrinoma in MEN1 had duodenal gastrinomas and 5 patien

72 Gastrinoma in MEN1 is considered a rarely curable diseas

73 Duodenal gastrinoma in MEN1 should be considered a surgically cur

74 tients with histologically proven metastatic gastrinoma in the liver with Zollinger-Ellison syndrome

75 Duodenal gastrinomas in patients with sporadic ZES are frequently

76 preoperative imaging study for extrahepatic gastrinomas in patients with ZES and should replace conv

77 herapy for the treatment of liver metastatic gastrinomas in the reduction of ZES.

78 In particular, the areas of gastrinoma, insulinoma, and multiple endocrine neoplasia

79 r nonhereditary tumors-parathyroid adenomas, gastrinomas, insulinomas, and bronchial carcinoids.

80 P-NETs, which include gastrinomas, insulinomas, and non-functioning tumours, o

81 nal imaging methods in the identification of gastrinomas later found at surgery (P = 0.004), but it s

82 gastrointestinal endocrine tumors including gastrinomas, little data are available on Chr 1 LOH, and

83 SRS detected 30% of gastrinomas < or =1.1 cm, 64% of those 1.1 to 2 cm, and

84 In patients with sporadic gastrinomas no clinical, laboratory, or radiographic loc

85 sults support the conclusion that primary LN gastrinomas occur and are not rare (approximately 10% of

86 monoclonal and that MEN1 gene alterations in gastrinomas occur before the development of tumor metast

87 as pancreatic, lymph node, and other primary gastrinomas occurred similarly.

88 Extrahepatic gastrinomas or liver metastases were identified by ultra

89 at factors contribute to failure to detect a gastrinoma, or whether the SRS result should be used to

90 Tumor types included parathyroid, gastrinoma, pancreatic endocrine, pituitary, and lung ca

91 tomy (Whipple procedure), lymph node primary gastrinoma, parietal cell vagotomy, reoperation and surg

92 From the literature, only a small number of gastrinoma patients treated with liver embolization for

93 survival, with one half of patients dying a gastrinoma-related death and none an acid-related death.

94 atient's medical history included pancreatic gastrinoma resected by means of left pancreatectomy 31 y

95 S patients who underwent routine surgery for gastrinoma/resection/cure was compared with 35 patients

96 received chemotherapy, and 13 had undergone gastrinoma resections without cure.

97 ological behavior of duodenal and pancreatic gastrinomas, role of imaging studies to localize tumor,

98 d human duodenal, lymph node, and pancreatic gastrinoma samples, collected from patients who underwen

99 e results of SRS for localizing extrahepatic gastrinomas should not be used to decide operability, be

100 rest is the observation that in the study of gastrinomas, SRS altered clinical management in almost 5

101 se a surgical procedure will detect 33% more gastrinomas than SRS.

102 endent mutations in MENIN were detected in a gastrinoma that also revealed LOH, leading to the possib

103 ccurred at 5 +/- 1 years, and 3 had duodenal gastrinoma that had been missed.

104 /- 0.1 (25% > or =1 LN), and 78% were in the gastrinoma triangle, which also did not differ from the

105 rs and routine removal of lymph nodes in the gastrinoma triangle.

106 ry, were analyzed with special regard to the gastrinoma type and the initial operative procedure.

107 Patients with pancreatic gastrinomas underwent either distal pancreatic resection

108 Thirteen patients with duodenal gastrinomas underwent PD resections (group 1, partial PD

109 The growth rate of metastatic gastrinoma varies markedly in different patients and 26%

110 At surgery, gastrinoma was found in 57 of 58 patients (98%).

111 Gastrinoma was found in 98% with DUODX compared with 76%

112 One hundred fifteen patients with gastrinoma were prospectively studied.

113 To address this issue, patients with gastrinomas were assessed.

114 Gastrinomas were detected in all patients at each surger

115 Gastrinomas were found in 141 of the patients (93 percen

116 Duodenal gastrinomas were found more frequently with DUODX (62% v

117 Seventy-four gastrinomas were found: 22 duodenal, 8 pancreatic, 3 pri

118 The majority of duodenal gastrinomas were in the first or second portions of the

119 At the time of diagnosis, 21 (77%) gastrinomas were malignant (18 duodenal, 3 pancreatic),

120 e tumors, all patients with liver metastatic gastrinomas were selected if treated with arterial embol

121 has only recently been recognized in a rare gastrinoma, where it was incapable of binding secretin o

122 MEN1-associated gastrinomas, which develop in the submucosa, might arise

123 hyperplasia precedes the appearance of MEN1 gastrinomas, which develop within submucosal Brunner's g

124 ce as well as identify a patient subset with gastrinomas who might benefit from trastuzumab treatment

125 cted MEN1 patients with biochemically proven gastrinoma, who underwent surgery, were analyzed with sp

126 focuses on the first case of coexistence of gastrinoma with neurofibromatosis type 2.

127 ocrine syndromes (insulinoma [hypoglycemia], gastrinoma [Zollinger-Ellison syndrome (ZES)], vasoactiv