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Genetic analysis of...
Genetic analysis of lithium-associated parathyroid tumors
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Dwight, T (författare)
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Kytola, S (författare)
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Teh, BT (författare)
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Theodosopoulos, G (författare)
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Richardson, AL (författare)
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Philips, J (författare)
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Twigg, S (författare)
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Delbridge, L (författare)
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Marsh, DJ (författare)
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Nelson, AE (författare)
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- Larsson, C (författare)
- Karolinska Institutet
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Robinson, BG (författare)
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(creator_code:org_t)
- Oxford University Press (OUP), 2002
- 2002
- Engelska.
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Ingår i: European journal of endocrinology. - : Oxford University Press (OUP). - 0804-4643 .- 1479-683X. ; 146:5, s. 619-627
- Relaterad länk:
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https://eje.bioscien...
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http://kipublication...
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https://doi.org/10.1...
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Abstract
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- OBJECTIVE: The aim of this study was to determine the primary genetic events that may underlie the formation of parathyroid tumors in patients with lithium-associated hyperparathyroidism (HPT). METHODS: Comparative genomic hybridization (CGH), loss of heterozygosity (LOH) and multiple endocrine neoplasia type 1 gene (MEN1) mutation analysis were used to analyze twelve parathyroid tumors from nine patients with lithium-associated HPT. For comparison, CGH was also carried out in a non-lithium-associated group of thirteen sporadic parathyroid tumors. RESULTS: A higher prevalence of multiglandular disease in the lithium-associated HPT patients compared with the idiopathic sporadic patients was observed (Fisher's exact test, P=0.02). CGH alterations were detected in four lithium-associated parathyroid tumors, involving loss at 1p, 11, 15q, 22q and gain of the X chromosome. In addition, one of these four cases exhibited LOH at 11q13 and was found to contain a novel somatic MEN1 mutation (c.1193insTAC). Although fewer lithium-associated parathyroid tumors were shown to contain genetic alterations compared with the sporadic parathyroid tumors, the changes detected were those frequently associated with both familial and sporadic parathyroid tumorigenesis. CONCLUSION: This is, to our knowledge, the first genetic analysis of parathyroid tumors in lithium-associated HPT patients. Our data indicated that the majority of lithium-associated parathyroid tumors do not contain gross chromosomal alterations and suggest that in most cases the tumorigenic pathway is independent of MEN1 and genes at 1p34.3-pter and 1q21-q32. It is possible that other discrete genetic alterations or epigenetic changes, not screened for in this study, could also be responsible for parathyroid tumorigenesis in lithium-associated HPT.
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Dwight, T
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Kytola, S
-
Teh, BT
-
Theodosopoulos, ...
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Richardson, AL
-
Philips, J
-
visa fler...
-
Twigg, S
-
Delbridge, L
-
Marsh, DJ
-
Nelson, AE
-
Larsson, C
-
Robinson, BG
-
visa färre...
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European journal ...
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Karolinska Institutet