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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
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
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
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
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
60 oendocrine tumors such as pheochromocytomas, paragangliomas, and the adrenocortical carcinomas (ACC),
61 stric GIST; a retroperitoneal, nonfunctional paraganglioma; and a mediastinal, catecholamine-secretin
63 ost cases of metastatic pheochromocytoma and paraganglioma are driven by dysregulation of the hypoxia
66 ms triggering metastasis in pheochromocytoma/paraganglioma are unknown, hindering therapeutic options
86 tations in the classic pheochromocytoma- and paraganglioma-associated genes (632 female [65.0%] and 3
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
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.
106 clinically characterize the pheochromocytoma/paraganglioma diseases associated with mutations of the
107 ovide excellent anatomic characterization of paragangliomas, gallium 68 tetraazacyclododecane tetraac
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
112 tiology for hereditary pheochromocytomas and paragangliomas has recently included SDHA, TMEM127, MAX,
116 ng modality in parasympathetic head and neck paragangliomas (HNPGLs) compared with anatomic imaging w
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
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
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
130 toma, embryonal and astrocytic brain tumors, paraganglioma, multiple endocrine neoplasia IIB, and neu
133 tations in patients presenting with multiple paragangliomas or somatostatinomas, and polycythemia.
136 PET has been increasingly used in imaging paraganglioma, paralleled by great efforts toward the de
140 = 4), myxoma (n = 3), teratoma (n = 2), and paraganglioma, pericardial cyst, Purkinje cell tumor, an
143 itary SDHB-mutant pheochromocytomas (PC) and paragangliomas (PG) are rare tumours with a high propens
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
153 aps within the critical region of hereditary paraganglioma (PGL1) on chromosomal band 11q23, we chara
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
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
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
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
178 se for treating metastatic pheochromocytomas/paragangliomas (PPGLs), a rare SSTR-expressing tumor.
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
187 N 2), the newly delineated phaeochromocytoma-paraganglioma syndrome and, less commonly, neurofibromat
189 very often associated with pheochromocytoma-paraganglioma syndromes, which are caused by mutations i
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
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
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
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
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