RET revisited: expanding the oncogenic portfolio

被引:403
作者
Mulligan, Lois M. [1 ,2 ]
机构
[1] Queens Univ, Canc Res Inst, Div Canc Biol & Genet, Kingston, ON K7L 3N6, Canada
[2] Queens Univ, Dept Pathol & Mol Med, Kingston, ON K7L 3N6, Canada
关键词
RECEPTOR TYROSINE KINASE; MEDULLARY-THYROID CARCINOMA; ENDOCRINE NEOPLASIA TYPE-2; CHRONIC MYELOMONOCYTIC LEUKEMIA; ENTERIC NERVOUS-SYSTEM; ACUTE MYELOID-LEUKEMIA; CANCER CELL INVASION; GDNF FAMILY LIGANDS; NEUROTROPHIC FACTOR; C-RET;
D O I
10.1038/nrc3680
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The RET receptor tyrosine kinase is crucial for normal development but also contributes to pathologies that reflect both the loss and the gain of RET function. Activation of RET occurs via oncogenic mutations in familial and sporadic cancers - most notably, those of the thyroid and the lung. RET has also recently been implicated in the progression of breast and pancreatic tumours, among others, which makes it an attractive target for small-molecule kinase inhibitors as therapeutics. However, the complex roles of RET in homeostasis and survival of neural lineages and in tumour-associated inflammation might also suggest potential long-term pitfalls of broadly targeting RET.
引用
收藏
页码:173 / 186
页数:14
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