CXCL12 catches T-ALL at the entrance of the bone marrow

Tatsuki Sugiyama; Takashi Nagasawa

doi:10.1016/j.it.2015.08.001

CXCL12 catches T-ALL at the entrance of the bone marrow

Trends Immunol. 2015 Sep;36(9):504-6. doi: 10.1016/j.it.2015.08.001. Epub 2015 Aug 14.

Authors

Tatsuki Sugiyama¹, Takashi Nagasawa²

Affiliations

¹ Department of Immunobiology and Hematology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan; Japan Science and Technology Agency (JST), Core Research for Evolutional Science and Technology (CREST), 53 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan.
² Department of Immunobiology and Hematology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan; Japan Science and Technology Agency (JST), Core Research for Evolutional Science and Technology (CREST), 53 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan. Electronic address: tnagasa@frontier.kyoto-u.ac.jp.

PMID: 26282886
DOI: 10.1016/j.it.2015.08.001

Abstract

A fraction of patients with T-cell acute lymphoblastic leukemias (T-ALLs) relapse and have a dismal prognosis. Two recent papers in Cancer Cell reveal that endothelial cell-derived CXCL12 is essential for bone marrow involvement and tumor progression in T-ALL patients, suggesting that this chemokine axis presents a potential therapeutic target for the treatment of T-ALL.

Publication types

Comment

MeSH terms

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*
Pyridines / pharmacology*

Substances

Chemokine CXCL12
Pyridines