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New driver of T cell leukemia growth

Date:
September 20, 2010
Source:
Rockefeller University Press
Summary:
NKX3.1, a protein that suppresses the development of prostate tumors, promotes the growth of a different type of tumor in the blood, according to new research.

NKX3.1, a protein that suppresses the development of prostate tumors, promotes the growth of a different type of tumor in the blood, according to a new study.

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The research was published online on September 20 in the Journal of Experimental Medicine.

Paul-Henri Romeo and colleagues find that TAL1, a protein abundantly expressed in approximately 40% of patients with T cell acute lymphoblastic leukemia (T-ALL), drives expression of NKX3.1. Eliminating NKX3.1 halted the growth of TAL1-expressing T-ALL cells in culture and after injection into mice.

It's not yet clear how NKX3.1 sustains the growth of T-ALL cells, but these findings show that this protein can either halt or hasten tumor development depending on the tissue environment.


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The above story is based on materials provided by Rockefeller University Press. Note: Materials may be edited for content and length.


Journal Reference:

  1. S. Kusy, B. Gerby, N. Goardon, N. Gault, F. Ferri, D. Gerard, F. Armstrong, P. Ballerini, J.-M. Cayuela, A. Baruchel, F. Pflumio, P.-H. Romeo. NKX3.1 is a direct TAL1 target gene that mediates proliferation of TAL1-expressing human T cell acute lymphoblastic leukemia. Journal of Experimental Medicine, 2010; 207 (10): 2141 DOI: 10.1084/jem.20100745

Cite This Page:

Rockefeller University Press. "New driver of T cell leukemia growth." ScienceDaily. ScienceDaily, 20 September 2010. <www.sciencedaily.com/releases/2010/09/100920123540.htm>.
Rockefeller University Press. (2010, September 20). New driver of T cell leukemia growth. ScienceDaily. Retrieved March 5, 2015 from www.sciencedaily.com/releases/2010/09/100920123540.htm
Rockefeller University Press. "New driver of T cell leukemia growth." ScienceDaily. www.sciencedaily.com/releases/2010/09/100920123540.htm (accessed March 5, 2015).

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