期刊
CANCER CELL
卷 30, 期 4, 页码 610-622出版社
CELL PRESS
DOI: 10.1016/j.ccell.2016.09.007
关键词
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资金
- German Research Council DFG [SFB 832-A16, KFO 286-RP6, KFO 286-RP5]
- Koln Fortune program of the University of Cologne [192/2013, 205/2013]
- Friedrich and Sophie Moritz'sche Stiftung
Survival of chronic lymphocytic leukemia (CLL) cells strictly depends on the support of an appropriate tumor microenvironment. Here, we demonstrate that LYN kinase is essential for CLL progression. Lyn deficiency results in a significantly reduced CLL burden in vivo. Loss of Lyn within leukemic cells reduces B cell receptor (BCR) signaling including BTK phosphorylation, but surprisingly does not affect leukemic cell expansion. Instead, syngeneic CLL transplantation of CLL cells into Lyn- or Btk-deficient recipients results in a strongly delayed leukemic progression and prolonged survival. Moreover, Lyn deficiency in macrophages hinders nursing functions for CLL cells, which is mediated by direct contact rather than secretion of soluble factors. Taken together, LYN and BTK seem essential for the formation of a microenvironment supporting leukemic growth.
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