T-Lymphoblastic Lymphoma Cells Express High Levels of BCL2, S1P1, and ICAM1, Leading to a Blockade of Tumor Cell Intravasation

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T-Lymphoblastic Lymphoma Cells Express High Levels of BCL2, S1P1, and ICAM1, Leading to a Blockade of Tumor Cell Intravasation

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Title: T-Lymphoblastic Lymphoma Cells Express High Levels of BCL2, S1P1, and ICAM1, Leading to a Blockade of Tumor Cell Intravasation
Author: Feng, Hui; Stachura, David L.; White, Richard; Gutierrez, Alejandro; Zhang, Lu; Sanda, Takaomi; Jette, Cicely A.; Testa, Joseph R.; Neuberg, Donna S.; Langenau, David M.; Kutok, Jeffery Lorne; Zon, Leonard Ira; Traver, David; Fleming, Mark Daniel; Kanki, John P.; Look, A. Thomas

Note: Order does not necessarily reflect citation order of authors.

Citation: Feng, Hui, David L. Stachura, Richard M. White, Alejandro Gutierrez, Lu Zhang, Takaomi Sanda, Cicely A. Jette, et al. 2010. T-Lymphoblastic Lymphoma Cells Express High Levels of BCL2, S1P1, and ICAM1, Leading to a Blockade of Tumor Cell Intravasation. Cancer Cell 18, no. 4: 353–366.
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Abstract: 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.
Published Version: doi:10.1016/j.ccr.2010.09.009
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3003429/pdf/nihms245604.pdf
Terms of Use: This article is made available under the terms and conditions applicable to Open Access Policy Articles, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#OAP
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:13041314
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