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1 MEN 2B patients, running a high risk of metastatic MTC,
8 ocrine neoplasia types 2A and 2B (MEN 2A and MEN 2B) and familial medullary thyroid carcinoma (FMTC),
11 ytoma (pheo), and hyperparathyroidism (HPT); MEN 2B, by MTC, pheo, and characteristic stigmata; and f
13 , cutaneous lesions classically described in MEN 2B syndrome, and 1 relative also showing multiple sc
19 Among 41 patients with de novo mutations, MEN 2B was diagnosed in 12 patients after recognition of
20 nts with de novo mutations when nonendocrine MEN 2B components are quickly appreciated and surgical i
21 bute to understanding the molecular basis of MEN 2B, and will assist in the clinical management of fa
22 918T, has been identified in 94% of cases of MEN 2B (which consists of MTC, pheochromocytoma and deve
25 nts with de novo mutations, the diagnosis of MEN 2B was triggered by symptomatic MTC (28 patients) or
27 rtained a patient with classical features of MEN 2B, but lacking either of the classical mutations in
32 ssion of a human Ret proto-oncogene with the MEN 2B mutation does not cause any features of MEN 2B in
33 the enhanced oncogenesis associated with the MEN 2B mutation may be due in part to alterations in rec
35 yndrome include macular amyloidosis, whereas MEN 2B syndrome is traditionally linked to multiple muco
36 ultiple endocrine neoplasia [MEN] 2A, 4 with MEN 2B, 1 each with von Hippel-Lindau and neurofibromato
41 sprung's disease (HD), and all patients with MEN 2B have intestinal neuromas and megacolon that can c
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