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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
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
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
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
38 oendocrine tumors such as pheochromocytomas, paragangliomas, and the adrenocortical carcinomas (ACC),
39 stric GIST; a retroperitoneal, nonfunctional paraganglioma; and a mediastinal, catecholamine-secretin
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.
61 clinically characterize the pheochromocytoma/paraganglioma diseases associated with mutations of the
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,
67 ng modality in parasympathetic head and neck paragangliomas (HNPGLs) compared with anatomic imaging w
70 tection and staging of pheochromocytomas and paragangliomas in different genotypes, including VHL-, S
73 90 individuals with pheochromocytomas and/or paragangliomas, including 898 previously unreported case
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
81 tations in patients presenting with multiple paragangliomas or somatostatinomas, and polycythemia.
84 PET has been increasingly used in imaging paraganglioma, paralleled by great efforts toward the de
87 = 4), myxoma (n = 3), teratoma (n = 2), and paraganglioma, pericardial cyst, Purkinje cell tumor, an
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
96 aps within the critical region of hereditary paraganglioma (PGL1) on chromosomal band 11q23, we chara
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
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
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
113 N 2), the newly delineated phaeochromocytoma-paraganglioma syndrome and, less commonly, neurofibromat
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
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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