PLK1 stabilizes a MYC-dependent kinase network in aggressive B cell lymphomas
| العنوان: | PLK1 stabilizes a MYC-dependent kinase network in aggressive B cell lymphomas |
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| المؤلفون: | Ji Yuan, Eduardo M. Sotomayor, Praneeth Reddy Sudalagunta, Bin Fang, Yuan Ren, Jianguo Tao, Chengfeng Bi, Julio C. Chavez, Kenneth H. Shain, Tint Lwin, William S. Dalton, Julie M. Vose, Lixin Wan, Kai Fu, Cheng Wang, Bijal D. Shah, Ariosto S. Silva, Xuefeng Wang, John M. Koomen, John L. Cleveland, Xiaohong Zhao, Lan V. Pham, Lynn C. Moscinski, Huijuan Jiang, Tao Li |
| المصدر: | Journal of Clinical Investigation. 128:5517-5530 |
| بيانات النشر: | American Society for Clinical Investigation, 2018. |
| سنة النشر: | 2018 |
| مصطلحات موضوعية: | Male, 0301 basic medicine, Regulator, Cell Cycle Proteins, Mice, SCID, Protein Serine-Threonine Kinases, Biology, PLK1, Proto-Oncogene Proteins c-myc, Mice, 03 medical and health sciences, Mice, Inbred NOD, Cell Line, Tumor, Proto-Oncogene Proteins, medicine, Animals, Humans, Kinome, B cell, Protein Stability, Cell growth, Kinase, General Medicine, medicine.disease, Lymphoma, 030104 developmental biology, medicine.anatomical_structure, Proteolysis, Commentary, Cancer research, Myeloid Cell Leukemia Sequence 1 Protein, Female, Lymphoma, Large B-Cell, Diffuse, Signal transduction, Signal Transduction |
| الوصف: | Inhibitors that target specific kinases or oncoproteins have become popular additions to or replacements for cytotoxic chemotherapies to treat many different types of cancer. However, many tumors lack a discernable target kinase and an amplified oncoprotein and/or rely on several cooperating mechanisms for progression. Thus, combinations of targeted therapies are essential for treating many cancers to avoid the rapid emergence of resistance. In this issue of the JCI, Ren et al. use an elegant kinase activity–profiling method and identify activity of the oncogene polo-like kinase-1 (PLK1) as an important driver of double-hit lymphoma (DHL), an aggressive subgroup of B cell lymphoma characterized by chromosomal translocations involving c-MYC and BCL2 or BCL6. Moreover, PLK1 activity was associated with MYC expression and poor prognosis in DHL patients. PLK1 inhibition with volasertib, alone and in combination with the BCL-2 inhibitor venetoclax, was efficacious in multiple DHL models, including mice harboring DHL patient–derived xenografts. Together, these data support PLK1 as a promising prognostic marker and therapeutic target for DHL. |
| تدمد: | 1558-8238 0021-9738 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d8d7a59fdd8110e53143502f7273815eTest https://doi.org/10.1172/jci122533Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....d8d7a59fdd8110e53143502f7273815e |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15588238 00219738 |
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