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| Open AccessIdentification of recurrent USP48 and BRAF mutations in Cushing’s disease
In this study the authors report USP48 and BRAF are frequently mutated in USP8 wild-type corticotroph adenomas, and cause Cushing’s disease mainly through promoting the promoter activity of POMC. Inhibition of BRAF may be a promising therapeutic strategy for the treatment of patients with BRAF-mutated corticotroph adenomas.
- Jianhua Chen
- , Xuemin Jian
- & Yongyong Shi
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Article |
Skp2 suppresses apoptosis in Rb1-deficient tumours by limiting E2F1 activity
The pRb target E2F1 possesses contradictory activities in promoting proliferation and apoptosis. Here, the authors define a pRb-Skp2-p27-cyclin A-E2F1 survival pathway that can be disrupted to prevent Rb1-deficient tumorigenesis in the pituitary intermediate lobe.
- Zhonglei Lu
- , Frederick Bauzon
- & Liang Zhu