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1 with aldestosterone adenomas and seven with phaeochromocytoma.
2 gioblastomas, renal cell carcinoma (RCC) and phaeochromocytoma.
3 an important cause of familial and isolated phaeochromocytoma.
4 ogically proven medullary thyroid cancer and phaeochromocytoma.
5 crest tumours such as neuroblastoma (NB) and phaeochromocytoma.
6 ed in one of the two patients with bilateral phaeochromocytoma.
7 ied in three of eight kindreds with familial phaeochromocytoma.
8 haemangioblastomas, renal cell carcinoma and phaeochromocytoma.
9 re included in our database, 563 of whom had phaeochromocytoma.
10 been found in approximately 10% of sporadic phaeochromocytomas.
11 genes for involvement in the pathogenesis of phaeochromocytomas.
12 only a minor role for GDNF in the genesis of phaeochromocytomas.
13 o contribute to the pathogenesis of sporadic phaeochromocytomas.
14 as, 12 MEN 2 phaeochromocytomas and five VHL phaeochromocytomas.
15 nce of somatic change in GDNF in 28 sporadic phaeochromocytomas, 12 MEN 2 phaeochromocytomas and five
16 in the pathogenesis of familial or sporadic phaeochromocytomas, allelic variation at the GDNF locus
20 hylation was found in 22% (5/23) of sporadic phaeochromocytomas and in 55% (37/67) of neuroblastomas
21 roup B, two patients with isolated bilateral phaeochromocytoma; and Group C, six cases of multiple ex
23 y characterise the outcomes of management of phaeochromocytoma associated with multiple endocrine neo
24 factors have been implicated in up to 10% of phaeochromocytoma cases, but recent data suggest that ge
27 multiple endocrine neoplasia type 2-related phaeochromocytoma continues to rely on adrenalectomies w
28 ns were identified in patients with familial phaeochromocytoma disease, but a c277C-->T (R93W) sequen
29 SGs in neural crest tumours, we (a) analysed phaeochromocytomas for 3p allele loss (n=41) and RASSF1A
30 r NF1: Group A, eight kindreds with familial phaeochromocytoma; Group B, two patients with isolated b
31 ne mutations in GDNF in 16 cases of familial phaeochromocytoma (groups A, B and C) and looked for evi
32 by which SDH subunit mutations predispose to phaeochromocytomas has not been defined in detail, but d
34 patients'RET genotype, type of treatment for phaeochromocytoma (ie, unilateral or bilateral operation
35 ed with multiple endocrine neoplasia type 2, phaeochromocytoma, is not as well characterised in terms
38 Group C, six cases of multiple extra-adrenal phaeochromocytoma or adrenal phaeochromocytoma with a fa
39 roup of patients with multiple extra-adrenal phaeochromocytoma or adrenal phaeochromocytoma with a fa
40 oplasia type 2 (MEN 2), the newly delineated phaeochromocytoma-paraganglioma syndrome and, less commo
41 ite development and up-regulation of trkA in phaeochromocytoma (PC(12)) cells in vitro confirmed NGF-
42 of lead on the nicotinic AChR in rat clonal phaeochromocytoma PC12 cells using whole-cell and single
44 detect exocytosis of catecholamines from rat phaeochromocytoma (PC12) cells in response to a reductio
45 ometric recordings were made from individual phaeochromocytoma (PC12) cells using carbon fibre microe
46 ing the cellular responses to hypoxia in rat phaeochromocytoma (PC12) cells, an oxygen-sensitive clon
47 ia also evoked secretion from chemoreceptive phaeochromocytoma (PC12) cells, which was wholly Ca2+ de
51 HABs) and renal cell carcinoma (RCC) but not phaeochromocytoma (PHE) occur in type 1 VHL disease.
54 ve been linked to the development of RCC and phaeochromocytoma, respectively, the precise basis for g
57 , germline SDHD and SDHB mutations may cause phaeochromocytoma susceptibility with or without associa
63 ever, 47 (57%) of 82 patients with bilateral phaeochromocytoma who underwent adrenal-sparing surgery
65 e extra-adrenal phaeochromocytoma or adrenal phaeochromocytoma with a family history of neuroectoderm
66 e extra-adrenal phaeochromocytoma or adrenal phaeochromocytoma with a family history of neuroectoderm
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