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 Barbouti, A. Articles by Fioretos, T. Search for Related Content PubMed PubMed Citation Articles by Barbouti, A. Articles by Fioretos, T.

A Novel Gene, MSI2, Encoding a Putative RNA-binding Protein Is Recurrently Rearranged at Disease Progression of Chronic Myeloid Leukemia and Forms a Fusion Gene with HOXA9 as a Result of the Cryptic t(7;17)(p15;q23)¹

Departments of Clinical Genetics [A. B., M. H., B. J., C. L., F. M., T. F.] and Hematology [P-G. N.], Lund University Hospital, SE-221 85 Lund, Sweden, and Department of Human Genetics, University of Leuven, Leuven, Belgium [A. H.]

The pathogenetic role of the P210 BCR/ABL1 fusion gene in the chronic phase of chronic myeloid leukemia (CML) has been well established.In contrast, the geneticmechanisms underlying the disease progression into the accelerated phase (AP) and the final blast crisis (BC) remain poorly understood. We have previously identified (A. Barbouti et al., Genes Chromosomes Cancer, 35: 127–137, 2002) two cryptic balanced translocations, t(7;17)(p15;q23) and t(7;17)(q32–34;q23), in CML AP/BC using multicolor fluorescence in situ hybridization. In this study, we show that a novel gene in 17q23, Musashi-2 (MSI2), encoding a putative RNA-binding protein, is rearranged in both cases and that a MSI2/HOXA9 fusion gene is formed in the case with the 7p15 breakpoint. The identified in-frame MSI2/HOXA9 fusion transcript retains both of the RNA recognition motif domains of MSI2, which is fused to the homeobox domain of HOXA9, and is likely to play an important role in the disease progression of CML.

This article has been cited by other articles:

				A. De Weer, F. Speleman, B. Cauwelier, N. Van Roy, N. Yigit, B. Verhasselt, B. De Moerloose, Y. Benoit, L. Noens, D. Selleslag, et al. EVI1 overexpression in t(3;17) positive myeloid malignancies results from juxtaposition of EVI1 to the MSI2 locus at 17q22 Haematologica, December 1, 2008; 93(12): 1903 - 1907. [Abstract] [Full Text] [PDF]

				L. Palmqvist, B. Argiropoulos, N. Pineault, C. Abramovich, L. M. Sly, G. Krystal, A. Wan, and R. K. Humphries The Flt3 receptor tyrosine kinase collaborates with NUP98-HOX fusions in acute myeloid leukemia Blood, August 1, 2006; 108(3): 1030 - 1036. [Abstract] [Full Text] [PDF]

				A. Subramanian, P. Tamayo, V. K. Mootha, S. Mukherjee, B. L. Ebert, M. A. Gillette, A. Paulovich, S. L. Pomeroy, T. R. Golub, E. S. Lander, et al. From the Cover: Gene set enrichment analysis: A knowledge-based approach for interpreting genome-wide expression profiles PNAS, October 25, 2005; 102(43): 15545 - 15550. [Abstract] [Full Text] [PDF]