| First Author | Yang Y | Year | 2022 |
| Journal | Biochem Biophys Res Commun | Volume | 626 |
| Pages | 51-57 | PubMed ID | 35970044 |
| Mgi Jnum | J:328132 | Mgi Id | MGI:7335686 |
| Doi | 10.1016/j.bbrc.2022.08.017 | Citation | Yang Y, et al. (2022) Induction of chronic lymphocytic leukemia-like disease in STYK1/NOK transgenic mice. Biochem Biophys Res Commun 626:51-57 |
| abstractText | 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. |
