期刊
CANCER CELL
卷 19, 期 6, 页码 740-753出版社
CELL PRESS
DOI: 10.1016/j.ccr.2011.05.007
关键词
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资金
- Deutsche Forschungsgemeinschaft
- Mildred-Scheel fellowship
- Deutsche Krebshilfe
- Fund for Scientific Research Flanders (FWO) [G.0651.08, G.0500.08]
- Federal Government Belgium [IUAP06/30]
- Flemish Government
- Concerted Research Activities, Stichting Emmanuel van der Schueren (Belgium) [GOA2006/11]
- Bijzonder Onderzoeks-fonds KUL [OT/08/037]
- Stichting tegen Kanker [SCIE2006-31]
- Center of Excellence (Mosaic) [EF/05/08]
- FWO-Vlaanderen
- APCL
- GSK
Imatinib has revolutionized the treatment of BCR-ABL1(+) chronic myeloid leukemia (CML), but, in most patients, some leukemia cells persist despite continued therapy, while others become resistant. Here, we report that PIGF levels are elevated in CML and that PIGF produced by bone marrow stromal cells (BMSCs) aggravates disease severity. CML cells foster a soil for their own growth by inducing BMSCs to upregulate PIGF, which not only stimulates BM angiogenesis, but also promotes CML proliferation and metabolism, in part independently of BCR-ABL1 signaling. Anti-PIGF treatment prolongs survival of imatinib-sensitive and -resistant CML mice and adds to the anti-CML activity of imatinib. These results may warrant further investigation of the therapeutic potential of PIGF inhibition for (imatinib-resistant) CML.
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