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RET 再探:扩展致癌基因谱。

RET revisited: expanding the oncogenic portfolio.

机构信息

Division of Cancer Biology and Genetics, Cancer Research Institute and Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario K7L 3N6, Canada.

出版信息

Nat Rev Cancer. 2014 Mar;14(3):173-86. doi: 10.1038/nrc3680.

Abstract

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.

摘要

RE 酪氨酸激酶受体对于正常发育至关重要,但也会导致功能丧失和获得的病理变化。RE 的激活是通过家族性和散发性癌症中的致癌突变引起的,最显著的是甲状腺癌和肺癌。RE 最近也被牵连到乳腺癌和胰腺癌等肿瘤的进展中,这使其成为小分子激酶抑制剂治疗的有吸引力的靶点。然而,RE 在神经谱系的稳态和存活以及肿瘤相关炎症中的复杂作用也可能表明广泛靶向 RET 的潜在长期风险。

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