دورية أكاديمية
Induction of chronic lymphocytic leukemia-like disease in STYK1/NOK transgenic mice.
| العنوان: | Induction of chronic lymphocytic leukemia-like disease in STYK1/NOK transgenic mice. |
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| المؤلفون: | Yang Y; Department of Pathogen Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China. Electronic address: yyboby0706@163.com., Liu L; Department of Pathogen Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & School of Basic Medicine, Peking Union Medical College, Beijing, 100005, China. Electronic address: lliu@mail.pumc.edu.cn., Tucker HO; Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, 1 University Station A5000, Austin TX, 78712, USA. Electronic address: haleytucker@austin.utexas.edu. |
| المصدر: | Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2022 Oct 20; Vol. 626, pp. 51-57. Date of Electronic Publication: 2022 Aug 08. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier Country of Publication: United States NLM ID: 0372516 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1090-2104 (Electronic) Linking ISSN: 0006291X NLM ISO Abbreviation: Biochem Biophys Res Commun Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: <2002- >: San Diego, CA : Elsevier Original Publication: New York, Academic Press. |
| مواضيع طبية MeSH: | Leukemia, Lymphocytic, Chronic, B-Cell*/genetics , Receptor Protein-Tyrosine Kinases*/metabolism, Animals ; Humans ; Mice ; Mice, Transgenic |
| مستخلص: | STYK1/NOK functions in a ligand independent and constitutive fashion to provoke tumor formation and to be up-regulated in many types of cancer cells. However, how STYK1/NOK functions at the whole animal level is completely unknown. Here, we found that STYK1/NOK-transgenic (tg) mice spontaneously developed immunosuppressive B-CLL-like disease with generally shorter life spans. The phenotype of STYK1/NOK-induced B-CLL was typically heterogeneous, and most often, presented lymphadenectasis accompanied with hepatomegaly and/or splenomegaly. STYK1/NOK-tg mice also suffered reduced immune responses. The expanded CD5 + CD19 + (B1) lymphocyte pool was detected within peripheral lymphoid organs. Analysis on GEO profile revealed that expression of STYK1/NOK were significantly up-regulated in primary human B-CLL. Inoculation of blood cells from sick STYK1/NOK-tg mice into immune-deficient recipients recaptured the B1 malignant phenotype. Our study demonstrated that STYK1/NOK transgenic mouse may serve as a useful model system for the developments of novel diagnosis and treatment of B-CLL. Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.) |
| فهرسة مساهمة: | Keywords: B lymphocyte; B1 cells; CLL; Lymphadenectasis; STYK1/NOK |
| المشرفين على المادة: | EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases) EC 2.7.10.2 (STYK1 protein, human) |
| تواريخ الأحداث: | Date Created: 20220815 Date Completed: 20220908 Latest Revision: 20221007 |
| رمز التحديث: | 20221213 |
| DOI: | 10.1016/j.bbrc.2022.08.017 |
| PMID: | 35970044 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1090-2104 |
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| DOI: | 10.1016/j.bbrc.2022.08.017 |