共 62 条
Clinical and molecular progress in hereditary paraganglioma
被引:68
作者:

Baysal, B. E.
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机构:
Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA
机构:
[1] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA
关键词:
D O I:
10.1136/jmg.2008.058560
中图分类号:
Q3 [遗传学];
学科分类号:
071007 ;
090102 ;
摘要:
Hereditary paraganglioma (PGL) is characterised by genetic predisposition to the development of highly vascular tumours of the paraganglionic tissues and caused by germ line inactivating mutations in the SDHB, SDHC and SDHD subunits of mitochondrial succinate dehydrogenase enzyme complex (SDH; mitochondrial complex II). Recent studies have demonstrated that SDH gene mutations in germ line occur in at least 11% of non-familial head and neck paragangliomas, 8% of non-familial pheochromocytomas, 28% of malignant pheochromocytomas and 33% of extra-adrenal pheochromocytomas. An increasing amount of data suggest that PGL mutations lead to constitutive activation of hypoxia signalling pathways. Genetic and structural models suggest that SDH mutations cause an accumulation of succinate and reactive oxygen species (ROS) which might act as downstream signalling molecules that activate hypoxia inducible pathways. However, many fundamental aspects of PGL pathogenesis, including the mechanism of ROS accumulation, the imprinted transmission pattern of SDHD mutations, and the precise role of SDH in regulation of oxygen homeostasis, remain poorly understood.
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页码:689 / 694
页数:6
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共 62 条
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