To elucidate further the genetic mechanisms for follicular thyroid tum
or development and progression, we allelotyped follicular thyroid tumo
rs and other thyroid lesions from 92 patients. In general, a low frequ
ency of loss of heterozygosity (LOH) was found, the highest being for
chromosomes 3q, 10q, 11p, 11q, 13q, and 22q (10%-15%). However, detail
ed study of LOH of these chromosome arms with regard to the different
histopathological diagnoses indicates that a locus on chromosome 10q m
ay be involved in follicular thyroid tumor progression. In addition, t
he majority of Hurthle cell adenomas showed LOH on either chromosome 3
q or 18q, in contrast to the other tumor types. This discrepancy in ge
netic alterations may contribute to the divergent clinical features oc
curring in these tumors.