0165-4608/00/$–see front matter PII S0165-4608(00)00213-2 Cancer Genet Cytogenet 121:99–100 (2000)  2000 Elsevier Science Inc. All rights reserved. 655 Avenue of the Americas, New York, NY 10010 LETTERS TO THE EDITOR Translocation (3;10)(q26;q22): A New Nonrandom Abnormality in Three Patients with 3q26 Involvement Acquired abnormalities of the long arm of chromosome 3 at q21 and q26 bands have been reported in 2–6% of pa- tients with myeloid malignancies, such as myeloprolifera- tive disorders, myelodysplastic syndromes (MDS), and acute myeloid leukemia (AML) [1–3]. This abnormality has been associated with several specific clinical and he- matological features, i.e. trilineage myelodysplasia, (par- ticularly abnormal megakaryocytes), additional abnormal- ities of chromosomes 7 and 5, resistance to chemotherapy, and poor prognosis [2–5]. Among 3q rearrangements, t(3;10) has been rarely reported. The purpose of this arti- cle is to describe three cases of t(3;10) with 10q22 rear- rangement, which has only been previously published in one case (search by MEDLINE from 1986 to 1999, key words: myeloproliferative disorders, myelodysplastic syn- dromes, myeloid leukemia, chromosome 3, as well as search in Mitelman’s Catalog of Chromosome Aberrations in Cancer, [6]). Three patients diagnosed with AML with t(3;10) (q26;q22) from a series of 296 AML cases diagnosed be- tween 1987 and 1998 in two Spanish hospitals are re- ported. The clinical and biological features are described in Table 1. The morphologic diagnoses of AML according to the FAB criteria were M1, M0, and M4. In all patients, trilineage myelodysplasia, mainly involving the mega- karyocytic series, was present at diagnosis. Intensive che- motherapy was administered to patients 1 and 2, being re- fractory. Patient 3 received palliative treatment only. At the time of this report, all patients have died, their sur- vival being 5, 18, and 8 months, respectively. Cytogenetic studies were performed at diagnosis on marrow aspirates of patients 1 and 3, and on peripheral blood of patient 2. Cells were cultured for 24 hours in cases 2 and 3, and analyzed by a direct method in case 1. G-banding was performed, and cytogenetic findings were described according to the ISCN guidelines [7]. Patient 1 presented three clones: 46,XY,t(3;10)(q26;q22)[4]/45,XY, t(3;10)(q26;q22), - 7 [6]/46,XY[5]. Patient 2 presented with 46,XY,t(3;10)(q26;q22)[24]. Patient 3 presented with t(3;10) (Fig. 1), monosomy 7, and deletion of chromosome 12: 45,XX,t(3;10)(q26;q22), - 7,del(12)(p11)[20]. The cyto- genetic studies were also performed at relapse in patients 1 and 2. Only patient 2 presented acquired abnormalities: t(5;12)(q15;p12) and monosomy 7, in addition to t(3;10). The paracentric inv(3)(q21q26) and the t(3;3)(q21;q26) are the most frequent rearrangements in 3q21q26 abnor- malities. Other 3q abnormalities, such as t(3;21)(q26;q21), t(1;3)(p36;q21), t(3;5)(q21;q23), and t(3;12)(q26;p13) [4] have been less frequently described. The activation of the EVl-1 gene is often present in chromosomal rearrange- ments involving band 3q26 [5]. Inappropriate expression of this gene has been shown in cases of inv(3), t(3;3), and in the other variants, such as t(3;21) and t(3;12) [8]. The t(3;10) is an infrequent 3q rearrangement. To our knowl- edge, only three cases of t(3;10) have been previously re- ported: t(3;10)(q21;q24) [9], t(3;10)(q29;q22) [10], and t(3;10)(q26;q11) [1]; the band 10q22 being present in only one of them. These three cases also had myeloid malig- nancies (secondary AML, biphenotypic leukemia, and MDS) and a poor prognosis. We report t(3;10)(q26;q22), a new nonrandom rear- rangement, in three patients with AML with typical clini- cobiologic characteristics of patients with 3q21q26 abnor- malities. Two features are of note: the first is the involvement of q22 in chromosome 10, which has been previously reported in one case [10], in which involve- ment of chromosome 3 was at band q29. The second is the constant involvement of chromosome 7 (monosomy) in our three cases, either at diagnosis or at relapse. Such a feature was not present in two of the three previously pub- lished cases [1, 10]. Supported in part by grants 97/1049 and 96/1332 from Fondo de Investigaciones Sanitarias, FIJC P-EF-98 from International José Carreras Leukemia Foundation, an Fundació per a la Recerca Biomèdica Germans Trias i Pujol. I. GRANADA Hematology Department E. LUÑO Hospital Universitat Germany Trias i Pujol J. M. RIBERA Universitat Autonoma de Barcelona C. SANZO Barcelona, Spain J. M. SANCHO Hematology Department S. G. MUÑIZ Hospital Central de Asturias F. MILLÁ Oviedo, Spain REFERENCES 1. Grigg AP, Gascoyne RD, Phillips GL, Horsman DE (1993): Clinical, haematological and cytogenetic features in 24 patients with structural rearrangements of q arm of chromo- some 3. Br J Haematol 83:158–165. 2. Fonstach C, Gudat H, Lenfelder E, Wandt H, Silling-Engel- hardt G, Ludwing W-D, Thiel E, Freud M, Bodenstein H, Schwieder G, Grüneisen A, Aul C, Schnittger S, Rieder H, Haase D, Hild F (1994): Correlation of cytogenetic findings