A new target in acute myeloid leukemia

Acute myeloid leukemia, a common leukemia in adults, is characterized by aberrant proliferation of cancerous bone marrow cells. Activating mutations in a protein receptor known as FLT3 receptor are among the most prevalent mutations observed in acute myeloid leukemias. FLT3 mutants are thought to activate several signaling pathways that contribute to cancer development.

Dr. Daniel Tenen and colleagues from Harvard University in Boston discovered a new pathway activated by FLT3 mutation. Their results show that cyclin dependent kinase 1 (CDK1), a critical regulator of cell division is activated in FLT3 mutated leukemias, leading to the activation of downstream .

Most importantly, they demonstrate that inhibiting CDK1 activity promotes differentiation of cells from patient-derived peripheral blood samples.

As clinical trials with CDK1 inhibitors are ongoing, their data strongly suggest that therapies targeting the CDK1 pathway may be efficacious for acute myeloid leukemias with FLT3 mutation, especially in patients resistant to FLT3 inhibitor therapies.


Explore further

FLT3 gene mutations play critically important role in acute myeloid leukemia

More information: Targeting CDK1 promotes FLT3-activated acute myeloid leukemia differentiation through C/EBPα, Journal of Clinical Investigation, 2012.
Citation: A new target in acute myeloid leukemia (2012, July 16) retrieved 24 June 2019 from https://medicalxpress.com/news/2012-07-acute-myeloid-leukemia.html
This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only.
 shares

Feedback to editors

User comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more