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1 nsitivity, followed by a discussion of their extrapancreatic actions, including effects on appetite a
2 ozantinib was 5% and 19% among patients with extrapancreatic and pancreatic neuroendocrine tumors, re
3 reatic solid tumours and history of previous extrapancreatic cancer underwent EUS-FNA from January/19
5 ions (DNA sequencing) and 11 were tested for extrapancreatic CFTR function (clinical and physiologic
7 , serum alkaline phosphatase, and absence of extrapancreatic cysts predict patients likely to progres
8 (85%) of 86 patients were taken to surgery, extrapancreatic disease was found in nine, and 64 (74%)
9 riteria for resectability: 1) the absence of extrapancreatic disease, 2) no tumor encasement of the s
10 50 hpf, a stage when the ventral bud-derived extrapancreatic duct is the main source of new endocrine
11 ntly increased beta-cell neogenesis near the extrapancreatic duct, demonstrating the feasibility of p
13 PR agonism to enhance the insulinotropic and extrapancreatic effects of GIP, thereby improving glycem
14 m of trypsin that is co-expressed in several extrapancreatic epithelial cells with ENaC, can activate
15 one marrow of diabetic rats, indicating that extrapancreatic, extrathymic insulin production occurs i
16 ad mutation in HNF1B even though the typical extrapancreatic features were not known at the time of r
18 s frequently part of a complex syndrome with extrapancreatic features: 18 genes causing syndromic neo
21 e developed independently for pancreatic and extrapancreatic gastrointestinal NETs, with novel therap
22 These findings emphasize the existence of extrapancreatic glucagon (perhaps originating from the g
26 larger median tumor diameter, higher rate of extrapancreatic invasion, and lower rate of pathologic m
27 that absence of an autoantigen in syngeneic extrapancreatic islet grafts in diabetic hosts renders t
31 inous neoplasm (IPMN) is infrequent and that extrapancreatic malignancies (EPMs) occur with unusual f
32 oma which are distinct from its influence in extrapancreatic malignancies and from the mechanistic ef
37 e criterion such as a threshold of 100 mL of extrapancreatic necrosis provides more reliable informat
38 significant relationships were found between extrapancreatic necrosis volume and organ failure, infec
40 nd intraobserver agreement in the grading of extrapancreatic necrosis was assessed by using kappa sta
42 The proportion of IPMN patients having any extrapancreatic neoplasm diagnosed before or coincident
43 as used to assess the risk of a diagnosis of extrapancreatic neoplasms among cases versus controls.
44 l studies have reported an increased risk of extrapancreatic neoplasms in patients with IPMN, but the
46 nic inflammation, and tumor metastases along extrapancreatic nerves are key features of pancreatic ma
47 (20 with pancreatic NETs [pNETs] and 20 with extrapancreatic NETs [epNETs]) treated at a tertiary car
48 in molecular genetics between pancreatic and extrapancreatic NETs, and studies are evaluating whether
49 e pancreas, intrapancreatic nerves, and some extrapancreatic neural pathways, with or without mediati
50 Patients with advanced, well-differentiated extrapancreatic neuroendocrine tumors (epNETs) have limi
51 independent cohorts of patients - those with extrapancreatic neuroendocrine tumors and those with pan
53 treatment of previously treated, progressive extrapancreatic or pancreatic neuroendocrine tumors is u
54 ith previously treated, progressive advanced extrapancreatic or pancreatic neuroendocrine tumors.
56 on histology, imaging, endoscopy, serology, extrapancreatic organ involvement, and response to stero
57 P are based on histology, imaging, serology, extrapancreatic organ involvement, and response to stero
58 1Rs) are also widely distributed in multiple extrapancreatic organs, providing a mechanistic explanat
59 le disease but have preoperative findings of extrapancreatic perineural invasion (EPNI) and/or duoden
60 ients, mesenteric vascular encasement in 14, extrapancreatic/peritoneal involvement in 16, and celiac
61 antation experiments showed that most of the extrapancreatic proinsulin-producing cells originated fr
63 biochemical phenotype that protects against extrapancreatic tissue injury to the lung, kidney and li
64 pancreatic adenocarcinomas, and other human extrapancreatic tissues and malignancies was examined, u
65 imens, 22 pancreatic adenocarcinomas, and 58 extrapancreatic tissues and tumors was subjected to RT-P
69 erglycemia inducing proinsulin expression in extrapancreatic tissues, we did not observe bioluminesce
70 imilar to protease, serine (PRSS) 3, a major extrapancreatic trypsinogen, was optimum at pH 8.0, and