Protein Kinase in Leukemia
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".
Deadline for manuscript submissions: closed (31 March 2021) | Viewed by 55076
Special Issue Editors
Interests: oncogenic signaling; kinases; leukemia; targeted therapies; resistance; stem cells
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Protein kinases are required to phosphorylate substrates on threonine, serine or tyrosine residues, allowing structural protein modification leading to enzyme activation or recruitments of signaling partners at docking sites, giving raise to signaling transduction pathways. About 500 human genes encode kinases. Kinase activity controls signaling pathways involved in many cellular processes, such as cell growth, proliferation, differentiation or metabolism. In hematopoiesis, many kinases play a key role at different steps of blood cell generation, and deregulation, through mutations, expression or location, often leads to malignancies. Among these, several chronic or acute leukemias are driven by deregulated kinases, for which recent decades have seen the development of targeted therapies. Although tyrosine phosphorylations represent only 0.1% of whole phosphorylation, deregulated tyrosine kinases are involved in a large number of oncogenic mechanisms.
Blocking kinase enzymatic activity has therefore become a quest for pharmaceutical companies. The paradigm of kinase targeting is remembered by the development of the first inhibitor FDA-approved in chronic myeloid leukemia (CML) treatment, imatinib.
Today, around 50 kinase inhibitors are FDA-approved, while at least 150 are being investigated in clinical trials.
Dr. Jean-Max Pasquet
Dr. Paulo De Sepulveda
Guest Editors
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Keywords
- Leukemia
- Kinase
- Oncogenic Signaling
- Targeted Therapies
- Resistance