Allelotyping of follicular thyroid tumors

J Zedenius, G Wallin, A Svensson, L Grimelius, A Höög… - Human genetics, 1995 - Springer
J Zedenius, G Wallin, A Svensson, L Grimelius, A Höög, G Lundell, M Bäckdahl, C Larsson
Human genetics, 1995Springer
To elucidate further the genetic mechanisms for follicular thyroid tumor development and
progression, we allelotyped follicular thyroid tumors and other thyroid lesions from 92
patients. In general, a low frequency of loss of heterozygosity (LOH) was found, the highest
being for chromosomes 3q, 10q, 11p, 11q, 13q, and 22q (10%–15%). However, detailed
study of LOH of these chromosome arms with regard to the different histopathological
diagnoses indicates that a locus on chromosome 10q may be involved in follicular thyroid …
Abstract
To elucidate further the genetic mechanisms for follicular thyroid tumor development and progression, we allelotyped follicular thyroid tumors and other thyroid lesions from 92 patients. In general, a low frequency of loss of heterozygosity (LOH) was found, the highest being for chromosomes 3q, 10q, 11p, 11q, 13q, and 22q (10%–15%). However, detailed study of LOH of these chromosome arms with regard to the different histopathological diagnoses indicates that a locus on chromosome 10q may be involved in follicular thyroid tumor progression. In addition, the majority of Hürthle cell adenomas showed LOH on either chromosome 3q or 18q, in contrast to the other tumor types. This discrepancy in genetic alterations may contribute to the divergent clinical features occurring in these tumors.
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