CXCL12 catches T-ALL at the entrance of the bone marrow.
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.
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.
Tatsuki
T
Sugiyama
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.
Takashi
T
Nagasawa
D000818:Animals; D054377:Chemokine CXCL12 / Q000037:antagonists & inhibitors* / Q000096:biosynthesis*; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D006801:Humans; D054218:Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / Q000188:drug therapy* / Q000378:metabolism*; D011725:Pyridines / Q000494:pharmacology*
D054377:Chemokine CXCL12; D011725:Pyridines