Multifaceted CK2 in malignant and healthy T cells

Copyright © Ribeiro et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and re-production in any medium, provided the original author and source are credited.Among kinases that support the survival and turnover of tumor cells, the serine/threonine protein kinase CK2 has been shown to be frequently overexpressed or hyperactivated in solid and hematological malignancies. Our previous work on T-cell acute lymphoblastic leukemia (T-ALL) showed that CK2 maintains leukemia cell viability by phosphorylating and thereby inactivating the tumor suppressor PTEN, which results in hyperactivation of PI3K/AKT signaling. We also demonstrated the potential of using the clinical-grade CK2-specific chemical inhibitor, CX-4945 (Silmitasertib), against primary T-ALL cells. We have now extended these findings to the rare (