T-ALL: Home Is where the CXCL12 Is

T cell acute lymphoblastic leukemia (T-ALL) is caused by mutations affecting cell survival, proliferation, and differentiation. In addition to requiring these mutations, Passaro and colleagues and Pitt and colleagues in this issue of Cancer Cell demonstrate that T-ALL initiating cells residing in bo...

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Bibliographic Details
Published in:Cancer cell 2015-06, Vol.27 (6), p.745-746
Main Authors: de Bock, Charles E., Cools, Jan
Format: Article
Language:English
Subjects:
Animals
Chemokine CXCL12 - antagonists & inhibitors
Chemokine CXCL12 - biosynthesis
Endothelium, Vascular - metabolism
Female
Humans
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - drug therapy
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - metabolism
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - pathology
Pyridines - pharmacology
Receptors, CXCR4 - metabolism
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Summary:T cell acute lymphoblastic leukemia (T-ALL) is caused by mutations affecting cell survival, proliferation, and differentiation. In addition to requiring these mutations, Passaro and colleagues and Pitt and colleagues in this issue of Cancer Cell demonstrate that T-ALL initiating cells residing in bone marrow depend on the CXCR4/CXCL12 signaling axis for disease maintenance and progression. T cell acute lymphoblastic leukemia (T-ALL) is caused by mutations affecting cell survival, proliferation, and differentiation. In addition to requiring these mutations, Passaro and colleagues and Pitt and colleagues in this issue of Cancer Cell demonstrate that T-ALL initiating cells residing in bone marrow depend on the CXCR4/CXCL12 signaling axis for disease maintenance and progression.
ISSN:1535-6108
1878-3686
DOI:10.1016/j.ccell.2015.05.011