期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 286, 期 1-2, 页码 180-186出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2007.08.013
关键词
pituitary adenoma; TSH-oma; acromegaly; somatostatin; somatostatin receptors; LOH
Somatostatin exerts antisecretive and antiproliferative effects on different endocrine cells by acting through a family of G protein-coupled receptors that includes five subtypes (SST1-5). Normal human pituitary and pituitary adenomas have been shown to express almost all SST subtypes, with the exception of SST4. Consistent with the observation that octreotide and other somatostatin analogs bind to SST2 and SST5 with high affinity, these genes have been screened for quantitative/qualitative abnormalities in tumors removed from patients with poor responsiveness to somatostatin analogs treatment. Data obtained in GH-secreting adenomas suggested that resistance to octreotide was frequently associated with low expression of SST2 mRNA, although other authors failed to confirm this finding. To date, the only mutational change involving SST2 and SST5 is the Arg to Trp substitution in codon 240 of the SST5 gene that was found in one acromegalic patient resistant to octreotide. Similarly, loss of heterozygosis at SST5 gene locus in pituitary adenomas has been described in individual tumors. In recent years, molecular studies investigated the possible association of gene polymorphisms and susceptibility to diseases and/or resistance to drugs. As far as polymorphic variants of SST genes are concerned, a possible role of SST5 C1004T and T-461C alleles in influencing GH and IGF-I levels in patients with acromegaly has been proposed. Nevertheless, polymorphic variants in SST2 and SST5 genes seem to have a minor, if any, role in determining the different responsiveness to somatostatin analogs in patients with acromegaly. (C) 2007 Published by Elsevier Ireland Ltd.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据