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1 ed primary or metastatic pheochromocytoma or paraganglioma.
2 of primary or metastatic pheochromocytoma or paraganglioma.
3 umor of the carotid body, which was likely a paraganglioma.
4 gene, were found in patients with hereditary paraganglioma.
5 n patients with advanced pheochromocytoma or paraganglioma.
6 rticipants with advanced pheochromocytoma or paraganglioma.
7 cificity in subtypes of pheochromocytoma and paraganglioma.
8 proved for patients with pheochromocytoma or paraganglioma.
9 f-function HIF2 mutations are also linked to paraganglioma.
10 metastatic or inoperable pheochromocytoma or paraganglioma.
11 itical threshold prevents the development of paraganglioma.
12 n neovascularization of pheochromocytoma and paraganglioma.
13  pVHL variants associated with a low risk of paraganglioma.
14 and hemangioblastomas without a high risk of paraganglioma.
15 riers (79%), particularly with head and neck paraganglioma.
16 ontribute to hereditary pheochromocytoma and paraganglioma.
17 with the third recurrence of retroperitoneal paraganglioma.
18  patients with suspected pheochromocytoma or paraganglioma.
19 gulare, 3 glomus tympanicum, and 1 laryngeal paraganglioma.
20 35 right, 1 bilateral); 2 were extra-adrenal paragangliomas.
21 ity with or without associated head and neck paragangliomas.
22 ear cell renal cell carcinomas (ccRCCs), and paragangliomas.
23 als to kidney cancer, hemangioblastomas, and paragangliomas.
24                Pheochromocytomas are adrenal paragangliomas.
25 s like neuroblastoma, pheochromocytomas, and paragangliomas.
26  to three patients harboring glomus jugulare paragangliomas.
27 and tumor size in patients with carotid body paragangliomas.
28 ad a deleterious SDHC mutation, which causes paragangliomas.
29  for known or suspected pheochromocytomas or paragangliomas.
30 e detection and staging of pheochromocytomas/paragangliomas.
31 , and 9 patients with extraadrenal abdominal paraganglioma (1 nonmetastatic, 8 metastatic), underwent
32 ial septal defect (24%), microcephaly (17%), paraganglioma (17%), and ovarian cancer (6.8%).
33 n were carotid paragangliomas (59) and vagal paragangliomas (27).
34 HNP were found; the most common were carotid paragangliomas (59) and vagal paragangliomas (27).
35 t DNMT3A PWWP domain mutations identified in paragangliomas(9) and microcephalic dwarfism(10) promote
36 ate with disease in a family with hereditary paraganglioma, a neuroendocrine tumor previously linked
37 hromocytomas occur and may be referred to as paragangliomas, although this term is also used to descr
38 of primary or metastatic pheochromocytoma or paraganglioma and 69 with suspected pheochromocytoma or
39 well-differentiated, nonfunctional malignant paraganglioma and a 70-y-old male patient with a metasta
40 he germ line of two families with hereditary paraganglioma and is conserved among four eukaryotic mul
41 tivity of (18)F-DOPA PET in the detection of paraganglioma and its metastatic lesions and to evaluate
42  activity was also measured in SDH-deficient paraganglioma and KIT mutant GIST; 4 of 34 patients (12%
43 ere associated with pheochromocytoma but not paraganglioma and occurred in an age group frequently ex
44 enting with paraganglioma and the other with paraganglioma and somatostatinoma, both of whom had poly
45 (HIF2A) in two patients, one presenting with paraganglioma and the other with paraganglioma and somat
46 e in the management of pheochromocytomas and paragangliomas and often guides treatment.
47 ncer (HLRCC), whereas mutations in SDH cause paragangliomas and phaeochromocytomas (HPGL).
48                                              Paragangliomas and pheochromocytomas are genetically het
49 ing, and follow-up indicated the presence of paragangliomas and pheochromocytomas in 68 patients and
50 nd a specificity of 88% for the detection of paragangliomas and pheochromocytomas on a patient basis
51             The average (18)F-DOPA uptake by paragangliomas and pheochromocytomas, expressed as a tum
52 imaging essay reviews the characteristics of paragangliomas and the use of multimodality imaging for
53 18)F-flubrobenguane in pheochromocytomas and paragangliomas and to investigate the biodistribution in
54 docrine tumors, especially in neuroblastoma, paraganglioma, and pheochromocytoma.
55 ients, 54 had PPGLs (40 pheochromocytomas, 7 paragangliomas, and 7 metastatic PPGLs), and 21 had non-
56 e have been linked to uterine leiomyomas and paragangliomas, and cancer cells have been shown to indu
57 aragangliomas, with a focus on head and neck paragangliomas, and discusses its impact on the manageme
58  SDHC) cause susceptibility to head and neck paragangliomas, and may be found in approximately 20% of
59 stinal stromal tumors (GISTs), extra-adrenal paragangliomas, and pulmonary chondromas.
60 oendocrine tumors such as pheochromocytomas, paragangliomas, and the adrenocortical carcinomas (ACC),
61 stric GIST; a retroperitoneal, nonfunctional paraganglioma; and a mediastinal, catecholamine-secretin
62 sitivity of (18)F-DOPA PET for metastases of paraganglioma appears to be limited.
63 ost cases of metastatic pheochromocytoma and paraganglioma are driven by dysregulation of the hypoxia
64                         Pheochromocytoma and paraganglioma are neoplasms originating in the adrenal m
65         The imaging features of gangliocytic paraganglioma are suggestive enough for the prospective
66 ms triggering metastasis in pheochromocytoma/paraganglioma are unknown, hindering therapeutic options
67                        Pheochromocytomas and paragangliomas are a rare tumor entity originating from
68                                  Most often, paragangliomas are benign and progress slowly, but metas
69                                              Paragangliomas are benign neuroendocrine tumors derived
70                        Pheochromocytomas and paragangliomas are genetically heterogeneous neural cres
71                   More than one-third of all paragangliomas are hereditary, reflecting the strong gen
72                                 Most cardiac paragangliomas are incidentally detected at echocardiogr
73                        Pheochromocytomas and paragangliomas are infrequent, genetically heterogeneous
74                                Head and neck paragangliomas are largely related to the pseudohypoxia
75                                              Paragangliomas are neuroendocrine tumors that derive fro
76         Whereas benign pheochromocytomas and paragangliomas are often successfully cured by surgical
77                                              Paragangliomas are rare neuroendocrine tumors of extra-a
78                                              Paragangliomas are rare neuroendocrine tumors that may a
79                        Pheochromocytomas and paragangliomas are rare tumors of chromaffin cell origin
80                                 Carotid body paragangliomas are rare tumors that often affect patient
81                                              Paragangliomas are typically located around the great ve
82                                              Paragangliomas arise from the sympathetic or parasympath
83 system, with the majority of parasympathetic paragangliomas arising in the head and neck.
84         A 49-year-old patient with bilateral paragangliomas around branches of carotid arteries.
85                        Pheochromocytomas and paragangliomas associated with succinate dehydrogenase (
86 tations in the classic pheochromocytoma- and paraganglioma-associated genes (632 female [65.0%] and 3
87     The tumor was diagnosed as a mediastinal paraganglioma at histologic assessment.
88    The PET/CT findings were grouped as HNPs, paraganglioma at other sites (non-HNPs), and metastatic
89 ts with HNPs and can demonstrate synchronous paragangliomas at other sites and distant metastases.
90 ma and 69 with suspected pheochromocytoma or paraganglioma based on symptoms of catecholamine excess,
91  paradigm in suspected pheochromocytomas and paragangliomas because of its homology with MIBG and the
92 cant difference in the prevalence of carotid paragangliomas between patients with SDHB and SDHD mutat
93 ct can be rescued by pVHL variants linked to paraganglioma, but not by pVHL variants associated with
94 e are tumor suppressor genes predisposing to paraganglioma, but only mutations in the SDHB subunit ar
95 specificity for imaging pheochromocytoma and paraganglioma, but with low sensitivity because of low s
96 metastatic or inoperable pheochromocytoma or paraganglioma by the U.S. Food and Drug Administration h
97 pheochromocytomas and extraadrenal abdominal paragangliomas by increasing the tumor-to-background rat
98 e coronary arteries should be determined, as paragangliomas can be perfused by the coronary arteries,
99 tients diagnosed with a phaeochromocytoma or paraganglioma carry a germline mutation in one of the su
100                      Given the lack of human paraganglioma cell lines, we studied the effects of inac
101 n for renal cell carcinoma, pheochromocytoma/paraganglioma, cerebral hemangioblastoma, and endolympha
102 adiopharmaceuticals for pheochromocytoma and paraganglioma (collectively named PPGLs) imaging, severa
103 ether the genotypes of pheochromocytomas and paragangliomas correlate with the uptake of (18)F-DOPA.
104 fter resection in patients with carotid body paragangliomas despite earlier intervention.
105                                              Paraganglioma develops from cells of the parasympathetic
106 clinically characterize the pheochromocytoma/paraganglioma diseases associated with mutations of the
107 ovide excellent anatomic characterization of paragangliomas, gallium 68 tetraazacyclododecane tetraac
108         The genes responsible for hereditary paragangliomas (glomus tumors, MIM No.
109 GIST without a personal or family history of paraganglioma had germline mutations in SDHB or SDHC.
110  colleagues describe DNA hypermethylation in paragangliomas harboring mutations in succinate dehydrog
111                       The molecular basis of paragangliomas has been investigated extensively in the
112 tiology for hereditary pheochromocytomas and paragangliomas has recently included SDHA, TMEM127, MAX,
113 etastatic or inoperable pheochromocytoma and paraganglioma, has resulted in renewed interest.
114 almost all VHL disease families that develop paraganglioma have missense VHL mutations.
115                     Hereditary head and neck paragangliomas (HNP) are very often associated with pheo
116 ng modality in parasympathetic head and neck paragangliomas (HNPGLs) compared with anatomic imaging w
117 ne evaluation of patients with head and neck paragangliomas (HNPs).
118      Histology confirmed pheochromocytoma or paraganglioma in 11 cases (8 adrenal, including 2 malign
119 tection and staging of pheochromocytomas and paragangliomas in different genotypes, including VHL-, S
120 difference in the frequency of head and neck paragangliomas in other locations was found.
121  of 63 (11%) malignant pheochromocytomas and paragangliomas in SDHA and TMEM127 disease.
122 olic processes seen in pheochromocytomas and paragangliomas, including (131)I/(123)I-metaiodobenzylgu
123 90 individuals with pheochromocytomas and/or paragangliomas, including 898 previously unreported case
124                               In most cases, paraganglioma is located around the common carotid arter
125 f adrenal pheochromocytomas and extraadrenal paragangliomas is unknown.
126 to gastrointestinal stromal tumor (GIST) and paraganglioma, is caused by germline mutations in succin
127 s associated with retention of extra-adrenal paraganglioma-like tissues resembling the fetal organ of
128 s with SDHD mutations more often had carotid paragangliomas located on the left side than on the righ
129            Metastatic phaeochromocytomas and paragangliomas (MPPGs) are orphan diseases.
130 toma, embryonal and astrocytic brain tumors, paraganglioma, multiple endocrine neoplasia IIB, and neu
131                            Carotid and vagal paragangliomas occurred most often.
132                        Pheochromocytomas and paragangliomas often exhibit dysregulation of glucose me
133 tations in patients presenting with multiple paragangliomas or somatostatinomas, and polycythemia.
134                            Pheochromocytomas/paragangliomas overexpress somatostatin receptors, and r
135  CBTs was higher than that of jugulotympanic paragangliomas (P = 0.026).
136    PET has been increasingly used in imaging paraganglioma, paralleled by great efforts toward the de
137                        Pheochromocytomas and paragangliomas (PCC/PGL) are the solid tumour type most
138 ar characterization of pheochromocytomas and paragangliomas (PCCs/PGLs), a rare tumor type.
139 inoma (HNSC) tumors and Pheochromocytoma and Paraganglioma (PCPG) tumors into distinct groups.
140  = 4), myxoma (n = 3), teratoma (n = 2), and paraganglioma, pericardial cyst, Purkinje cell tumor, an
141      Introduction Pheochromocytoma (PCC) and paraganglioma (PG) research is limited due to rarity of
142                   Pheochromocytomas (PC) and paragangliomas (PG) are rare neuroendocrine tumors assoc
143 itary SDHB-mutant pheochromocytomas (PC) and paragangliomas (PG) are rare tumours with a high propens
144                                   Hereditary paraganglioma (PGL) is characterized by the development
145 ve SDH subunit genes predisposes to familial paraganglioma (PGL) or pheochromocytoma (PHEO).
146 hromosome band 11q23, cause highly penetrant paraganglioma (PGL) tumors when transmitted through fath
147 /= two distinct types of tumors, one of them paraganglioma (PGL), is unusual in an individual patient
148 me complex, succinate dehydrogenase (SDH) in paraganglioma (PGL), it has become clear that some cells
149 dehydrogenase (SDHB) predispose to malignant paraganglioma (PGL).
150 ts with metastatic pheochromocytoma (PC) and paraganglioma (PGL).
151 mical hallmark of pheochromocytoma (PCC) and paraganglioma (PGL).
152                     Hereditary nonchromaffin paragangliomas (PGL; glomus tumors; MIM 168000) are most
153 aps within the critical region of hereditary paraganglioma (PGL1) on chromosomal band 11q23, we chara
154  signatures in pheochromocytomas (PHEOs) and paragangliomas (PGLs).
155 with metastatic pheochromocytomas (PCCs) and paragangliomas (PGLs).
156 and metastatic pheochromocytomas (PHEOs) and paragangliomas (PGLs).
157  on monocytes isolated from pheochromocytoma/paraganglioma (PHEO) patients.
158 ; and a mediastinal, catecholamine-secreting paraganglioma (pheochromocytoma).
159  the parasympathetic and sympathetic system (paragangliomas, pheochromocytoma) and other very rare lo
160 fractory stage 4 neuroblastoma or metastatic paraganglioma/pheochromocytoma (MP) were treated using a
161 MIBG has essentially been only palliative in paraganglioma/pheochromocytoma patients.
162 en patients (5 with neuroblastoma and 5 with paraganglioma/pheochromocytoma) received 148-444 MBq (4-
163 euroendocrine tumors, such as neuroblastoma, paraganglioma/pheochromocytoma, and carcinoids; and disc
164                                Patients with paragangliomas, pheochromocytomas and neuroblastomas wer
165 ighly sensitive method for pheochromocytomas/paragangliomas (PHEOs/PGLs) associated with succinate de
166 atients with pheochromocytoma or sympathetic paraganglioma (PPGL) develop metastatic disease, most of
167 unresectable (advanced) pheochromocytoma and paraganglioma (PPGL) have poor prognoses and few treatme
168                             Pheochromocytoma/paraganglioma (PPGL) syndromes associated with polycythe
169                         Pheochromocytoma and Paraganglioma (PPGL) tumours with known genetic aetiolog
170 reditary tumors such as pheochromocytoma and paraganglioma (PPGL), renal cell carcinoma, and gastroin
171 oses to the development of phaeochromocytoma/paraganglioma (PPGL), wild type gastrointestinal stromal
172 f the genetic basis of phaeochromocytoma and paraganglioma (PPGL).
173 uation of patients with pheochromocytoma and paraganglioma (PPGL).
174                       Phaeochromocytomas and paragangliomas (PPGL) are rare neuroendocrine tumours th
175                        Pheochromocytomas and paragangliomas (PPGLs) can be localized by (18)F-FDG PET
176                        Pheochromocytomas and paragangliomas (PPGLs) present diagnostic challenges due
177                        Pheochromocytomas and paragangliomas (PPGLs) provide some of the clearest gene
178 se for treating metastatic pheochromocytomas/paragangliomas (PPGLs), a rare SSTR-expressing tumor.
179 current or metastatic phaeochromocytomas and paragangliomas (PPGLs).
180 al characterization of pheochromocytomas and paragangliomas (PPGLs).
181                                              Paragangliomas rarely involve the heart, and they accoun
182 alignant pheochromocytoma, neuroblastoma, or paraganglioma receiving [(131)I]MIBG treatment, as well
183  up European-American-Asian Pheochromocytoma-Paraganglioma Registry for prevalence of SDHA, TMEM127,
184 yndrome in some circumstances and to cancer (paraganglioma, renal cell carcinoma, gastrointestinal st
185 r patients underwent 41 primary carotid body paraganglioma resections (median follow-up time of 42 mo
186 y identified as a novel pheochromocytoma and paraganglioma susceptibility gene.
187 N 2), the newly delineated phaeochromocytoma-paraganglioma syndrome and, less commonly, neurofibromat
188 enase subunits SDHB-D cause pheochromocytoma-paraganglioma syndrome.
189  very often associated with pheochromocytoma-paraganglioma syndromes, which are caused by mutations i
190 e endocrine neoplasia-2 (MEN2), and familial paraganglioma syndromes.
191 mean) was seen for both pheochromocytoma and paraganglioma than for healthy adrenal glands (11.9 +/-
192 mean) was seen for both pheochromocytoma and paraganglioma than for healthy adrenal glands (11.9 2.0
193 y advanced or metastatic pheochromocytoma or paraganglioma that was not amenable to surgery or curati
194  in a patient with polycythemia and multiple paragangliomas (the Pacak-Zhuang syndrome).
195 ing is now recommended for all patients with paragangliomas to provide screening and surveillance rec
196 enetic mutations alter the aggressiveness of paragangliomas, treatment decisions are currently based
197 nate dehydrogenase; SDH) genes predispose to paraganglioma tumors that show constitutive activation o
198 adrenal (pheochromocytoma) and extraadrenal (paraganglioma) tumors, sensitivities were 88% and 67%, r
199                              At MRI, cardiac paragangliomas typically have low to intermediate signal
200  patients with suspected pheochromocytoma or paraganglioma underwent PET/CT or PET/MRI at 63 +/- 24 m
201  patients with suspected pheochromocytoma or paraganglioma underwent PET/CT or PET/MRI at 63 24 min a
202 t-Hogg-Dube Syndrome, Carcinoma, Renal Cell, Paragangliomas, Urinary, Kidney (C) RSNA, 2024.
203 utation-related metastatic pheochromocytomas/paragangliomas using (68)Ga-DOTATATE PET/CT.
204 gs in five patients with proved gangliocytic paraganglioma were reviewed.
205 GIST without a personal or family history of paraganglioma were tested for SDH germline mutations.
206 ing approaches used in pheochromocytomas and paragangliomas, which vary among clinical and genotypic
207 of patients with metastatic pheochromocytoma/paraganglioma who presented with a primary tumor in chil
208 modialysis-dependent patient with metastatic paraganglioma who was treated with [(131)I]MIBG.
209 ve analysis of 34 patients with carotid body paragangliomas who underwent genetic testing and surgica
210 colon cancer, 1 lung cancer, and 1 malignant paraganglioma) who underwent separate (18)F PET/CT and (
211  discuss the therapy of pheochromocytoma and paraganglioma with (131)I-MIBG and (90)Y- or (177)Lu-DOT
212 radionuclide therapy of pheochromocytoma and paraganglioma with (90)Y- or (177)Lu-DOTA conjugated som
213 who present with metastatic pheochromocytoma/paraganglioma with primary tumor development in childhoo
214 -line imaging in patients with head and neck paragangliomas with concern for multifocal and metastati
215 e introduces the molecular classification of paragangliomas, with a focus on head and neck paragangli

 
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