Molecular genetics of multiple endocrine neoplasia types 1 and 2.
Six multiple endocrine neoplasia (MEN) syndromes have received a level of attention that might seem disproportionate to their low prevalence. The attention has been given because their hormonal excesses cause striking metabolic expressions and because they might clarify pathways disrupted in more common tumours. The recent discovery of the main gene in each MEN syndrome has furthered our understanding of not only hereditary but also sporadic tumours and has fostered new avenues of research.
Marx
Stephen J
SJ
National Institutes of Health, Building 10, Room 9C-101, Bethesda, Maryland 20892-1802, USA. StephenM@intra.niddk.nih.gov
D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D051379:Mice; D018761:Multiple Endocrine Neoplasia Type 1 / Q000235:genetics*; D018813:Multiple Endocrine Neoplasia Type 2a / Q000235:genetics*; D009154:Mutation; D015513:Oncogene Proteins / Q000235:genetics; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000502:physiology; D051096:Proto-Oncogene Proteins c-ret; D020794:Receptor Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000235:genetics
C105373:MEN1 protein, human; D015513:Oncogene Proteins; D011518:Proto-Oncogene Proteins; D051096:Proto-Oncogene Proteins c-ret; C099282:RET protein, human; D020794:Receptor Protein-Tyrosine Kinases