PubMed Health⌕ Search

PubMed · 11977533

[Multiple endocrine neoplasia].

Abstract

In multiple endocrine neoplasia (MEN) syndromes, tumors appear either synchronously or heterochronously in a combination of 2 or more specified endocrine glands. They are broadly classified as MEN 1 or MEN 2 according to the combination of tumors, and are inherited as an autosomal dominant trait. The genes responsible for these syndromes have been identified, making early diagnosis based on familial screening possible. The gene responsible for MEN 1 is located on the long arm of chromosome 11. It is a tumor suppressor gene that codes for menin. The cause of MEN 2 type is a mutation of the RET proto-oncogene on the long arm of chromosome 10. The present article discusses the diagnosis and treatment of these syndromes.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Hiroshi Takami, Yoshifumi Ikeda, Kaori Kameyama. 2002. [Multiple endocrine neoplasia].. https://pubmed.ncbi.nlm.nih.gov/11977533/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Depletion of vesicle-tethering factor p115 causes mini-stacked Golgi fragments with delayed protein transport.

Depletion of p115 with small interfering RNA caused fragmentation of the Golgi apparatus, resulting in dispersed distribution of stacked short cisternae and a vesicular structure (mini-stacked Golgi). The mini-stacked Golgi with cis- and trans-organization is functional in protein transport and glycosylation, although secretion is considerably retarded in p115 knockdown cells. The fragmented Golgi was further disrupted by treatment with breferdin A and reassembled into the mini-stacked Golgi by removal of the drug, as observed in control cells. In addition, p115 knockdown cells maintained retrograde transport from the Golgi to the endoplasmic reticulum, although the rate was not as efficient as in control cells. While no alternation of microtubule networks was found in p115 knockdown cells, the fragmented Golgi resembled those in cells treated with anti-microtubule drugs. The results suggest that p115 is involved in vesicular transport between endoplasmic reticulum and the Golgi, along with microtubule networks.

Drosophila Proteins↗

Conserved mechanisms of signal transduction by Toll and Toll-like receptors.

In recent years, considerable progress has been made towards understanding the mechanism by which endotoxin is detected by the cells of the immune system. Lipopolysaccharides are extracted in a soluble form by the serum LPS binding protein and then transferred sequentially to the extrinsic membrane protein CD14 and the co-receptor complex TLR4/MD-2. Our modelling studies suggest that acyl chains of lipid A are buried within the hydrophobic core of MD-2 and this induces cross-linking of the two TLR4/MD-2 complexes, an event that is required to trigger signal transduction. We also propose that, by analogy with the Drosophila Toll receptor, the mechanism of signal transduction is likely to be complex and to involve concerted protein conformational changes. In particular, we propose that receptor-receptor interactions mediated by juxtamembrane sequences play a critical role.

Drosophila Proteins↗