T-lymphoblastic lymphoma cells express high levels of BCL2, S1P1, and ICAM1, leading to a blockade of tumor cell intravasation.

Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.

Cancer cell 2010 Oct 19

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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. Copyright © 2010 Elsevier Inc. All rights reserved.

Citation

Hui Feng, David L Stachura, Richard M White, Alejandro Gutierrez, Lu Zhang, Takaomi Sanda, Cicely A Jette, Joseph R Testa, Donna S Neuberg, David M Langenau, Jeffery L Kutok, Leonard I Zon, David Traver, Mark D Fleming, John P Kanki, A Thomas Look. T-lymphoblastic lymphoma cells express high levels of BCL2, S1P1, and ICAM1, leading to a blockade of tumor cell intravasation. Cancer cell. 2010 Oct 19;18(4):353-66