Cancer Genetics and Cytogenetics 157 (2005) 90–91

Letter to the editor

Y-chromosome loss in acute promyelocytic leukemia

Y-chromosome loss (�Y) may be seen as an age-relatedphenomenon in bone marrow (BM) cells of normal males[1], but it also occurs as a primary cytogenetic abnormality[2], as well as a secondary change, particularly in acutemyeloid leukemia (AML) with t(8;21) [3].

Since 1986 we have found 4 male patients with acutepromyelocytic leukemia (APL) whose ages did not exceed60 years, with �Y in their BM cells. This change was seenin 1.62% of all male APL patients (247 cases) receivingcytogenetic examination in our hospital. Among them, 3 hadt(15;17)(q22;q21) and one had t(11;17)(q23;q21). Specifi-cally, a 13-year-old boy had a 45,X,�Y,t(15;17)(q22;q21)[15]/46,XY[10] (Fig. 1). Interphase fluorescence in situ hy-bridization (I-FISH) using a centromere-specific probe forthe Y-chromosome labeled with SpectrumRed did not showa red signal in 72% (144/200) of his BM cells, indicating a�Y anomaly. At the same time, dual-color FISH using locus-specific probes for the PML and RARα genes, which werelabeled by SpectrumGreen and SpectrumOrange, respec-tively, showed one green, one orange, and one yellow(fusion) signal in 93% (186/200) of his BM cells, indicatingfusion of PML and RARα genes. For this case, �Y cannotbe related to his age; on the contrary, it may be involved inthe neoplastic process. During the same period, weencountered 109 male cases with t(8;21) in AML with a

Fig. 1. R-banded karyotype: 45,X,�Y,t(15;17)(q22;q21).

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�Y anomaly, who accounted for 50% of all male t(8;21)AML (218 cases) examined in our hospital.

On reviewing the literature, we found 7 cases of maleAPL patients with a �Y anomaly whose ages were below60 years [3–9]. Among them, 5 had t(15;17) and 2 hadt(11;17). Thus, we consider that although loss of the Y-chromosome is predominantly associated with the t(8;21)AML, it may also be present in rare male APL patients witht(15;17) or t(11;17). However, the reason for the associationbetween �Y and specific translocations remains unknown.

Yafang WuYongquan Xue

Jinlan PanLeukemia Research Unit

Jiangsu Institute of HematologyThe First Affiliated Hospital of Soochow University

Suzhou 215006People’s Republic of China

Acknowledgments

This work was supported by grant ZS0201 from the Scien-tific Technological Bureau of Suzhou, People’s Republicof China.

References

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[3] Rowley JD. Recurring chromosome abnormalities in leukemia.Semin Hematol 1990;27:122–36.

[4] Au WY, Ma SK, Lam CC, Chan LC, Kwong YL. Tetraploid acutepromyelocytic leukemia with large bizarre blast cell morphology.Cancer Genet Cytogenet 1999;115:52–5.

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Letter to the editor / Cancer Genetics and Cytogenetics 157 (2005) 90–91 91

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