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1 umor of the carotid body, which was likely a paraganglioma.
2 gene, were found in patients with hereditary paraganglioma.
3 riers (79%), particularly with head and neck paraganglioma.
4 ontribute to hereditary pheochromocytoma and paraganglioma.
5 n neovascularization of pheochromocytoma and paraganglioma.
6 with the third recurrence of retroperitoneal paraganglioma.
7 gulare, 3 glomus tympanicum, and 1 laryngeal paraganglioma.
8 ed primary or metastatic pheochromocytoma or paraganglioma.
9 of primary or metastatic pheochromocytoma or paraganglioma.
10 35 right, 1 bilateral); 2 were extra-adrenal paragangliomas.
11 ity with or without associated head and neck paragangliomas.
12  to three patients harboring glomus jugulare paragangliomas.
13 and tumor size in patients with carotid body paragangliomas.
14 ad a deleterious SDHC mutation, which causes paragangliomas.
15  for known or suspected pheochromocytomas or paragangliomas.
16 e detection and staging of pheochromocytomas/paragangliomas.
17 , and 9 patients with extraadrenal abdominal paraganglioma (1 nonmetastatic, 8 metastatic), underwent
18 n were carotid paragangliomas (59) and vagal paragangliomas (27).
19 HNP were found; the most common were carotid paragangliomas (59) and vagal paragangliomas (27).
20 ate with disease in a family with hereditary paraganglioma, a neuroendocrine tumor previously linked
21 hromocytomas occur and may be referred to as paragangliomas, although this term is also used to descr
22 of primary or metastatic pheochromocytoma or paraganglioma and 69 with suspected pheochromocytoma or
23 he germ line of two families with hereditary paraganglioma and is conserved among four eukaryotic mul
24 tivity of (18)F-DOPA PET in the detection of paraganglioma and its metastatic lesions and to evaluate
25  activity was also measured in SDH-deficient paraganglioma and KIT mutant GIST; 4 of 34 patients (12%
26 ere associated with pheochromocytoma but not paraganglioma and occurred in an age group frequently ex
27 enting with paraganglioma and the other with paraganglioma and somatostatinoma, both of whom had poly
28 (HIF2A) in two patients, one presenting with paraganglioma and the other with paraganglioma and somat
29 ncer (HLRCC), whereas mutations in SDH cause paragangliomas and phaeochromocytomas (HPGL).
30                                              Paragangliomas and pheochromocytomas are genetically het
31 ing, and follow-up indicated the presence of paragangliomas and pheochromocytomas in 68 patients and
32 nd a specificity of 88% for the detection of paragangliomas and pheochromocytomas on a patient basis
33             The average (18)F-DOPA uptake by paragangliomas and pheochromocytomas, expressed as a tum
34 docrine tumors, especially in neuroblastoma, paraganglioma, and pheochromocytoma.
35 e have been linked to uterine leiomyomas and paragangliomas, and cancer cells have been shown to indu
36  SDHC) cause susceptibility to head and neck paragangliomas, and may be found in approximately 20% of
37 stinal stromal tumors (GISTs), extra-adrenal paragangliomas, and pulmonary chondromas.
38 oendocrine tumors such as pheochromocytomas, paragangliomas, and the adrenocortical carcinomas (ACC),
39 stric GIST; a retroperitoneal, nonfunctional paraganglioma; and a mediastinal, catecholamine-secretin
40 sitivity of (18)F-DOPA PET for metastases of paraganglioma appears to be limited.
41         The imaging features of gangliocytic paraganglioma are suggestive enough for the prospective
42                                  Most often, paragangliomas are benign and progress slowly, but metas
43                                              Paragangliomas are benign neuroendocrine tumors derived
44                        Pheochromocytomas and paragangliomas are genetically heterogeneous neural cres
45                        Pheochromocytomas and paragangliomas are infrequent, genetically heterogeneous
46                                              Paragangliomas are rare neuroendocrine tumors that may a
47                        Pheochromocytomas and paragangliomas are rare tumors of chromaffin cell origin
48                                 Carotid body paragangliomas are rare tumors that often affect patient
49         A 49-year-old patient with bilateral paragangliomas around branches of carotid arteries.
50                        Pheochromocytomas and paragangliomas associated with succinate dehydrogenase (
51 tations in the classic pheochromocytoma- and paraganglioma-associated genes (632 female [65.0%] and 3
52    The PET/CT findings were grouped as HNPs, paraganglioma at other sites (non-HNPs), and metastatic
53 ts with HNPs and can demonstrate synchronous paragangliomas at other sites and distant metastases.
54 ma and 69 with suspected pheochromocytoma or paraganglioma based on symptoms of catecholamine excess,
55 cant difference in the prevalence of carotid paragangliomas between patients with SDHB and SDHD mutat
56 pheochromocytomas and extraadrenal abdominal paragangliomas by increasing the tumor-to-background rat
57 n for renal cell carcinoma, pheochromocytoma/paraganglioma, cerebral hemangioblastoma, and endolympha
58 ether the genotypes of pheochromocytomas and paragangliomas correlate with the uptake of (18)F-DOPA.
59 fter resection in patients with carotid body paragangliomas despite earlier intervention.
60                                              Paraganglioma develops from cells of the parasympathetic
61 clinically characterize the pheochromocytoma/paraganglioma diseases associated with mutations of the
62         The genes responsible for hereditary paragangliomas (glomus tumors, MIM No.
63 GIST without a personal or family history of paraganglioma had germline mutations in SDHB or SDHC.
64  colleagues describe DNA hypermethylation in paragangliomas harboring mutations in succinate dehydrog
65 tiology for hereditary pheochromocytomas and paragangliomas has recently included SDHA, TMEM127, MAX,
66                     Hereditary head and neck paragangliomas (HNP) are very often associated with pheo
67 ng modality in parasympathetic head and neck paragangliomas (HNPGLs) compared with anatomic imaging w
68 ne evaluation of patients with head and neck paragangliomas (HNPs).
69      Histology confirmed pheochromocytoma or paraganglioma in 11 cases (8 adrenal, including 2 malign
70 tection and staging of pheochromocytomas and paragangliomas in different genotypes, including VHL-, S
71 difference in the frequency of head and neck paragangliomas in other locations was found.
72  of 63 (11%) malignant pheochromocytomas and paragangliomas in SDHA and TMEM127 disease.
73 90 individuals with pheochromocytomas and/or paragangliomas, including 898 previously unreported case
74                               In most cases, paraganglioma is located around the common carotid arter
75 f adrenal pheochromocytomas and extraadrenal paragangliomas is unknown.
76 to gastrointestinal stromal tumor (GIST) and paraganglioma, is caused by germline mutations in succin
77 s with SDHD mutations more often had carotid paragangliomas located on the left side than on the righ
78 toma, embryonal and astrocytic brain tumors, paraganglioma, multiple endocrine neoplasia IIB, and neu
79                            Carotid and vagal paragangliomas occurred most often.
80                        Pheochromocytomas and paragangliomas often exhibit dysregulation of glucose me
81 tations in patients presenting with multiple paragangliomas or somatostatinomas, and polycythemia.
82                            Pheochromocytomas/paragangliomas overexpress somatostatin receptors, and r
83  CBTs was higher than that of jugulotympanic paragangliomas (P = 0.026).
84    PET has been increasingly used in imaging paraganglioma, paralleled by great efforts toward the de
85                        Pheochromocytomas and paragangliomas (PCC/PGL) are the solid tumour type most
86 ar characterization of pheochromocytomas and paragangliomas (PCCs/PGLs), a rare tumor type.
87  = 4), myxoma (n = 3), teratoma (n = 2), and paraganglioma, pericardial cyst, Purkinje cell tumor, an
88                                   Hereditary paraganglioma (PGL) is characterized by the development
89 ve SDH subunit genes predisposes to familial paraganglioma (PGL) or pheochromocytoma (PHEO).
90 hromosome band 11q23, cause highly penetrant paraganglioma (PGL) tumors when transmitted through fath
91 /= two distinct types of tumors, one of them paraganglioma (PGL), is unusual in an individual patient
92 me complex, succinate dehydrogenase (SDH) in paraganglioma (PGL), it has become clear that some cells
93 mical hallmark of pheochromocytoma (PCC) and paraganglioma (PGL).
94 dehydrogenase (SDHB) predispose to malignant paraganglioma (PGL).
95                     Hereditary nonchromaffin paragangliomas (PGL; glomus tumors; MIM 168000) are most
96 aps within the critical region of hereditary paraganglioma (PGL1) on chromosomal band 11q23, we chara
97  signatures in pheochromocytomas (PHEOs) and paragangliomas (PGLs).
98 with metastatic pheochromocytomas (PCCs) and paragangliomas (PGLs).
99 and metastatic pheochromocytomas (PHEOs) and paragangliomas (PGLs).
100 ; and a mediastinal, catecholamine-secreting paraganglioma (pheochromocytoma).
101  the parasympathetic and sympathetic system (paragangliomas, pheochromocytoma) and other very rare lo
102 fractory stage 4 neuroblastoma or metastatic paraganglioma/pheochromocytoma (MP) were treated using a
103 MIBG has essentially been only palliative in paraganglioma/pheochromocytoma patients.
104 en patients (5 with neuroblastoma and 5 with paraganglioma/pheochromocytoma) received 148-444 MBq (4-
105 euroendocrine tumors, such as neuroblastoma, paraganglioma/pheochromocytoma, and carcinoids; and disc
106 ighly sensitive method for pheochromocytomas/paragangliomas (PHEOs/PGLs) associated with succinate de
107                             Pheochromocytoma/paraganglioma (PPGL) syndromes associated with polycythe
108 uation of patients with pheochromocytoma and paraganglioma (PPGL).
109                        Pheochromocytomas and paragangliomas (PPGLs) can be localized by (18)F-FDG PET
110  up European-American-Asian Pheochromocytoma-Paraganglioma Registry for prevalence of SDHA, TMEM127,
111 r patients underwent 41 primary carotid body paraganglioma resections (median follow-up time of 42 mo
112 y identified as a novel pheochromocytoma and paraganglioma susceptibility gene.
113 N 2), the newly delineated phaeochromocytoma-paraganglioma syndrome and, less commonly, neurofibromat
114 enase subunits SDHB-D cause pheochromocytoma-paraganglioma syndrome.
115  very often associated with pheochromocytoma-paraganglioma syndromes, which are caused by mutations i
116 enetic mutations alter the aggressiveness of paragangliomas, treatment decisions are currently based
117 nate dehydrogenase; SDH) genes predispose to paraganglioma tumors that show constitutive activation o
118 adrenal (pheochromocytoma) and extraadrenal (paraganglioma) tumors, sensitivities were 88% and 67%, r
119 utation-related metastatic pheochromocytomas/paragangliomas using (68)Ga-DOTATATE PET/CT.
120 gs in five patients with proved gangliocytic paraganglioma were reviewed.
121 GIST without a personal or family history of paraganglioma were tested for SDH germline mutations.
122 of patients with metastatic pheochromocytoma/paraganglioma who presented with a primary tumor in chil
123 ve analysis of 34 patients with carotid body paragangliomas who underwent genetic testing and surgica
124 colon cancer, 1 lung cancer, and 1 malignant paraganglioma) who underwent separate (18)F PET/CT and (
125 who present with metastatic pheochromocytoma/paraganglioma with primary tumor development in childhoo

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