Yifei Qin
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Yifei Qin has a total of 5 co-authors. Here are the top co-authors by number of shared publications:
Glenn Merlino
Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, USA
1 shared publication- Lei Huang
State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China; CAMS Key Laboratory of Small Molecule Immuno-Oncology Drug Discovery, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China
1 shared publication Liping Huang
Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, USA
1 shared publication- Qiang Zuo
Department of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China
1 shared publication - Yanlin Yu
Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
1 shared publication
Latest Publications
- Open Access
- 19 July 2021
- Published by Springer Nature in npj Precision Oncology
- Vol. 5 (1) , 1-9
PERK mediates resistance to BRAF inhibition in melanoma with impaired PTEN
Targeting mutant BRAF in patients with melanomas harboring this oncogene has been highly successful as a first-line treatment, but other mutations may affect its efficacy and alter the route of acquired resistance resulting in recurrence and poor prognosis. As an evolving strategy, melanoma treatment needs to be expanded to include targets based on newly discovered emerging molecules and pathways. We here show that PERK plays a critical role in BRAF inhibitor-acquired resistance in melanoma with impaired PTEN. Inhibition of PERK by either shRNA or a pharmacological inhibitor blocked the growth of BRAF inhibitor-resistant melanoma with impaired PTEN in vitro and in vivo, suggesting an effective approach against melanomas with mutant BRAF and PTEN deficiency. Our current findings, along with our previous discovery that the AXL/AKT axis mediates resistance to BRAF inhibition in melanoma with wild-type PTEN, provide new insights toward a strategy for combating BRAF inhibition-acquired resistance in BRAF mutant melanoma with different PTEN statuses.
- 19 July 2021
- Published by Springer Nature in npj Precision Oncology
- Vol. 5 (1) , 1-9
Open AccessPERK mediates resistance to BRAF inhibition in melanoma with impaired PTEN
Targeting mutant BRAF in patients with melanomas harboring this oncogene has been highly successful as a first-line treatment, but other mutations may affect its efficacy and alter the route of acquired resistance resulting in recurrence and poor prognosis. As an evolving strategy, melanoma treatment needs to be expanded to include targets based on newly discovered emerging molecules and pathways. We here show that PERK plays a critical role in BRAF inhibitor-acquired resistance in melanoma with impaired PTEN. Inhibition of PERK by either shRNA or a pharmacological inhibitor blocked the growth of BRAF inhibitor-resistant melanoma with impaired PTEN in vitro and in vivo, suggesting an effective approach against melanomas with mutant BRAF and PTEN deficiency. Our current findings, along with our previous discovery that the AXL/AKT axis mediates resistance to BRAF inhibition in melanoma with wild-type PTEN, provide new insights toward a strategy for combating BRAF inhibition-acquired resistance in BRAF mutant melanoma with different PTEN statuses.