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• W2016925447 abstract "To the Editor, Synovial sarcoma X breakpoint 2 (SSX2) (Tureci et al, 1996) is a member of a highly conserved family of SSX genes that are only expressed in the testis and at very low levels in the thyroid gland of normal individuals. SSX2 is also expressed in various cancer types including approximately 50% of melanomas (Tureci et al, 1996). SSX2 interacting protein (SSX2IP) was identified through it’s interaction with SSX2 in a yeast two-hybrid system and was suggested to regulate the function of SSX2 in the testes and malignant cells (de Bruijn et al, 2002). We have previously shown that SSX2IP expression was elevated in 33% of acute myeloid leukaemia (AML) patient samples at presentation (Guinn et al, 2005) and that expression peaked on the surface of myeloid leukaemia cells during mitosis (Denniss et al, 2007). Using published microarray data (Bullinger et al, 2004), we analysed 116 adult patients with acute myeloid leukaemia (AML), and found that SSX2IP was underexpressed in patients with a t(8;21) translocation and overexpressed in patients harbouring a t(15;17) translocation (P < 0·001, one-way analysis of variance)(Fig 1A). There was a positive correlation between SSX2IP expression and FLT3-internal tandem repeat (P = 0·008, t-test) but not white blood cell count, sex, age or survival. We then examined an independent dataset containing 118 adult AML patients analysed using the U133plus2.0 chip. All six probe sets that related to SSX2IP expression were consistently lower in patients with a t(8;21) translocation (data not shown). SSX2IP expression in acute myeloid leukaemia patients. Gene expression profiling demonstrated that (A)SSX2IP expression was elevated in patients harbouring the t(15;17) translocation and decreased in patients harbouring the t(8;21) translocation. Box-and-Whisker plots in which the Y-axis shows the log2 transformed, mean-centred SSX2IP expression ratios; (B) SSX2IP was expressed at low levels, as was CDC20, in patients harbouring a t(8;21) translocation as compared with patients without this translocation and normal bone marrow donors (NBM). Data was generated using principal component analysis, axes show normalized intensities of the probe sets. Acute promyelocytic leukaemia (APL) is characterized by a t(15;17) translocation, which leads to the PML-retinoic acid receptor alpha (RARα) product. PML is a nuclear matrix-associated phosphoprotein whose expression is regulated during the cell cycle, its overexpression has been shown to lead to G1 arrest in normal fibroblasts and this function is thought to be lost when PML becomes attached to RARα. Our studies showed that a large number of genes involved in the cell cycle were upregulated in APL patients with a statistically significant correlation with the upregulated SSX2IP expression observed. Of particular note were genes encoding proteins involved in regulating cyclin dependent kinase (CDK) activity (p57Kip2, cdk7, cyclins D2, D3, E2 and B2), DNA replication (Cdc6) and mitosis [survivin and centromere protein J (CENPJ)]. The t(8;21) translocation is found in 12% of de novo AML cases and in up to 40% of patients with the AML M2 subtype and leads to the acute myeloid leukaemia 1 (AML1)-ETO fusion product. In a recent paper, Boyapati et al (2007) described a mouse model of t(8;21) in which cells harboured a C-terminal truncated AML-ETO product (named AEtr), which is almost identical to the AML1-ETO exon 9a isoform expressed in AML patients. Primary cells and cell lines harbouring AEtr-developed aneuploidy through the attenuation of the spindle checkpoint. The authors suggested that the reduced levels of spindle checkpoint proteins may contribute to the aneuploidy seen in t(8;21) leukaemia patients. When we examined our microarray datasets for associations between SSX2IP and the genes involved in spindle checkpoints described by Boyapati et al (2007), we found a strong correlation between low-CDC20 expression, one of the substrate-targeting subunits of the anaphase-promoting complex (APC), and low-SSX2IP expression in patients harbouring t(8;21) when compared with AML patients without a t(8;21) translocation (P < 0·0001) and normal donors (P < 0·0001) (Fig 1B). It should be noted that some of the genes (PTTG1, BUB1B and ESPL1) investigated by Boyapati et al (2007) were not present on the U133plus2.0 chip. In summary, our data shows that SSX2IP is affected in two ways that relate to the cell cycling of AML cells. In patients harbouring the t(15;17) translocation, overexpression of SSX2IP is associated with an abnormal elevation in the expression of genes involved in cell cycle. Conversely, in AML cells harbouring the t(8;21) translocation, the low levels of SSX2IP are associated with low levels of CDC20 protein, part of the APC which is thought to contribute to the development of aneuploidy seen in these patients. We would like to thank Mrs Amanda Gilkes for technical assistance. B.G. is funded by Leukaemia Research Fund, L.B. and J.G. received grants from the German José Carreras Leukaemia Foundation (DJCLS RO5/22) and the German Research Fund (DFG, GR2676/1-1) and N.S.B. received grants from the Leukaemia Research Fund and Medical Research Council." @default.
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• W2016925447 date "2007-11-19" @default.
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• W2016925447 title "SSX2IP expression in acute myeloid leukaemia: an association with mitotic spindle failure in t(8;21), and cell cycle in t(15;17) patients" @default.
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• W2016925447 doi "https://doi.org/10.1111/j.1365-2141.2007.06892.x" @default.
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