期刊
CANCER CELL
卷 18, 期 4, 页码 353-366出版社
CELL PRESS
DOI: 10.1016/j.ccr.2010.09.009
关键词
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资金
- National Institutes of Health [CA068484, K99CA134743, NRSA T32-HL086344, 1K08CA133103, 1K01DK074555, CA077429, K01AR05562190-01A1, 3K01AR055619-03S1]
- Leukemia & Lymphoma Society
- Prevent Cancer Foundation
- William Lawrence Foundation
- Harvard Stem Cell Institute
The molecular events underlying the progression of T-lymphoblastic lymphoma (T-LBL) to acute T-lymphoblastic leukemia (T-ALL) remain elusive. In our zebrafish model, concomitant overexpression of bcl-2 with Myc accelerated T-LBL onset while inhibiting progression to T-ALL. The T-LBL cells failed to invade the vasculature and showed evidence of increased homotypic cell-cell adhesion and autophagy. Further analysis using clinical biopsy specimens revealed autophagy and increased levels of BCL2, S1P1, and ICAM1 in human T-LBL compared with T-ALL. Inhibition of S1P1 signaling in T-LBL cells led to decreased homotypic adhesion in vitro and increased tumor cell intravasation in vivo. Thus, blockade of intravasation and hematologic dissemination in T-LBL is due to elevated S1P1 signaling, increased expression of ICAM1, and augmented homotypic cell-cell adhesion.
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