This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hayashi, Y. Articles by Nakahata, T. Search for Related Content PubMed PubMed Citation Articles by Hayashi, Y. Articles by Nakahata, T.

SN-1, A Novel Leukemic Cell Line with t(11;16)(q23;p13): Myeloid Characteristics and Resistance to Retinoids and Vitamin D₃¹

Department of Pediatrics, Faculty of Medicine, University of Tokyo, Tokyo 113-8655 [Y. Ha., T. T., F. B., M. Y.]; Department of Chemotherapy, Saitama Cancer Center Research Institute, Saitama 362-0806 [Y. Ho., N. N.]; Department of Pediatrics, Osaka City General Hospital, Osaka 534-0021 [M. S.]; Department of Pediatrics, Keio University School of Medicine, Tokyo 160-0016 [T. M.]; and Department of Clinical Oncology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639 [K. T., T. N.], Japan

The MLL gene is fused with the cAMP-responsive element binding protein-binding protein (CBP) gene in t(11;16)(q23;p13), which has been reported to be associated with therapy-related acute leukemia. We established a novel myeloid cell line, SN-1, from a patient with T-cell acute lymphoblastic leukemia with t(11;16)(q23;p13) having in-frame MLL-CBP fusion transcripts. The majority of the SN-1 cells were positive for myeloperoxidase when examined using an electron microscope and expressed CD13, CD33, CD56, and HLA-DR antigens, but not CD7, CD10, CD19, CD34, or CD41 antigens, suggesting that these cells are of myeloid origin. SN-1 cells underwent functional and morphological differentiation when treated with actinomycin D or sodium butyrate, but not with all-trans-retinoic acid (ATRA) or 1,25-dihydroxyvitamin D₃ (VD3). Exposure of SN-1 cells to ATRA hardly affected cell growth and differentiation, whereas the growth of HL-60 and NB4 cells treated with ATRA was effectively inhibited, and differentiation into mature granulocytes was induced. SN-1 cells were relatively insensitive to VD3 with respect to inhibiting the cell growth and inducing the ability to reduce nitroblue tetrazolium, lysozyme activity, and morphological differentiation, although the expression of CD11b was slightly induced by VD3. These results suggest that the cell line was impaired in the signal transduction systems of ATRA and VD3. This cell line should be useful for the study of the role of CBP as a transcriptional regulator in leukemia differentiation and for the functional analysis of the MLL-CBP fusion gene, which will provide new insights into leukemogenesis caused by 11q23 translocations.

This article has been cited by other articles:

				X.-J. Yang The diverse superfamily of lysine acetyltransferases and their roles in leukemia and other diseases Nucleic Acids Res., February 11, 2004; 32(3): 959 - 976. [Abstract] [Full Text] [PDF]

				Md. M. Rahman, A. Kukita, T. Kukita, T. Shobuike, T. Nakamura, and O. Kohashi Two histone deacetylase inhibitors, trichostatin A and sodium butyrate, suppress differentiation into osteoclasts but not into macrophages Blood, May 1, 2003; 101(9): 3451 - 3459. [Abstract] [Full Text] [PDF]

				T. Taketani, T. Taki, N. Shibuya, E. Ito, J. Kitazawa, K. Terui, and Y. Hayashi The HOXD11 Gene Is Fused to the NUP98 Gene in Acute Myeloid Leukemia with t(2;11)(q31;p15) Cancer Res., January 1, 2002; 62(1): 33 - 37. [Abstract] [Full Text] [PDF]

				S. Schreiner, M. Birke, M.-P. Garcia-Cuellar, O. Zilles, J. Greil, and R. K. Slany MLL-ENL Causes a Reversible and myc-dependent Block of Myelomonocytic Cell Differentiation Cancer Res., September 1, 2001; 61(17): 6480 - 6486. [Abstract] [Full Text] [PDF]