- Email: [email protected]
Jumping translocation of chromosome 1q associated with good clinical outcome in a case of Burkitt leukemia
Cancer Genetics 204 (2011) 207e210
BRIEF COMMUNICATION
Jumping translocation of chromosome 1q associated with good clinical outcome in a case of Burkitt leukemia Beata Bessenyei a,*, Aniko Ujfalusi a, Erzsebet Balogh a, Eva Olah a, Istvan Szegedi b, Csongor Kiss b a
Clinical Genetic Center, Department of Pediatrics, University of Debrecen Medical and Health Science Center, Debrecen, Hungary; b Division of Hematology, Department of Pediatrics, University of Debrecen Medical and Health Science Center, Debrecen, Hungary Acquired jumping translocations (JTs) are rare secondary aberrations occurring in various hematological malignancies. In Burkitt lymphoma/leukemia (BL) chromosome 1q abnormalities such as partial or whole arm duplications/translocations are frequently associated with the diseasespecific t(8;14)(q24;q32). JTs of 1q are considered to have a bad prognostic impact in BL. We report clinical, conventional and molecular cytogenetic findings of a 12-year-old boy who presented with BL. In addition to the primary aberration, t(8;14)(q24;q32), JT of 1q onto chromosomes 21 and der(14) as well as the formation of isochromosome 1q could be detected in his bone marrow sample. Despite the expected poor prognostic outcome of these aberrations, the patient has been experiencing an event free survival of 7.5 years at the time of the present report, reflecting the excellent clinical outcome of the disease. Keywords Jumping translocation, 1q, Burkitt leukemia, mFISH ª 2011 Elsevier Inc. All rights reserved.
Jumping translocations (JTs) are rare cytogenetic aberrations involving a donor chromosome arm or segment that is fused to two or more different recipient chromosomes in different cell lines of the same patient (1). They may be constitutional or acquired rearrangements and occur in various pathologic conditions. JTs are rare aberrations in hematological malignancies, but they have been described in various diseases including acute myeloid leukemia (AML) M1 and M5, BCR/ABL positive acute lymphoblastic leukemia (ALL), myelodysplastic syndrome (MDS), multiple myeloma (MM) and Burkitt lymphoma/leukemia (BL) (2e5). An extra copy of chromosome 1q is a common secondary aberration in Burkitt leukemia associated with L3 morphology of lymphoblasts, mature B-cell immunophenotype (sIg) and with the specific translocation, t(8;14)(q24;q32) or its variants, t(8;22)(q24;q11) and t(2;8)(p12;q24). An extra copy of 1q usually originates from a translocated unbalanced derivate chromosome, an isochromosome or a jumping translocation. JT of 1q have usually been reported to be Received February 18, 2010; received in revised form September 2, 2010; accepted October 27, 2010. * Corresponding author. E-mail address: [email protected] 2210-7762/$ - see front matter ª 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.cancergencyto.2010.10.005
associated with a poor clinical outcome (1). Hereby, we present a case with a JT of 1q associated with a good prognosis in a case of Burkitt leukemia with atypical late preB cell immunophenotype and t(8;14)(q24;q32) translocation.
Materials and methods Patient A 12-year-old boy sought care for weakness, headache, fever, and skin suffusions. At admission, peripheral blood tests revealed a white blood cell count of 27.6 109/L, hemoglobin of 112 g/L, and platelet count of 19 109/L. A bone marrow aspirate showed 50% blasts with Frenche AmericaneBritish L3 morphology. Immunophenotyping of the blasts by flow cytometry identified atypical, late pre-B-cell phenotype with CD10, CD19, CD45, CD71, cyCD79a, and cy IgM antigen expression. Blasts were negative for surface immunoglobulin light chains. Lumbar puncture was performed, and the results revealed no evidence of atypical cells in the cerebrospinal fluid. Cytogenetic analysis showed a t(8;14)(q24;q32) and a jumping translocation of 1q. Based on the morphology and the immunophenotype of the blasts
208 along with cytogenetic data, a diagnosis of Burkitt leukemia was made. Cytostatic therapy according to the non-Hodgkin €nster group trial (NHL BFM lymphoma Berlin-Frankfurt-Mu 95, branch II, R4) was introduced. The patient experienced complete hematologic and cytogenetic remission, which was maintained for 7.5 years after the diagnosis.
Cytogenetic analysis Conventional cytogenetic analysis was performed on bone marrow leukocytes at the time of diagnosis after a 24-hourlong culture by standard techniques and was evaluated
B. Bessenyei et al. by G banding. Twenty metaphases were analyzed and the karyotype was described according to the International System for Human Cytogenetic Nomenclature (ISCN, 2009).
Fluorescence in situ hybridization (FISH) analysis FISH studies were performed on bone marrow cytogenetic specimens at diagnosis using the following commercial DNA probes: LSI IGH/MYC, CEP8 (Abbott Molecular, Des Plaines, IL); 1pter and 1qter subtelomere specific probes (Cytocell, Cambridge, UK); 24XCyte multicolor FISH (mFISH) probe kit (MetaSystems, Altlussheim, Germany). All probes
Figure 1 (A) Partial G-banded and multicolor fluorescence in situ hybridization (mFISH) karyograms of two cells showing der(1) and i(1)(q10) besides the two normal chromosomes 1. mFISH clarified that der(1) resulted from a t(1;21)(q10;p10) and confirmed the i(1)(q10). Arrows indicate the abnormal chromosomes. (B) Interphase FISH using IGH/MYC probes shows one normal IGH (green) signal, one normal MYC (orange) signal, and two fusion signals indicating a t(8;14)(q24;q32). (C) mFISH karyogram of the third cell line showing 46,XY,der(14)t(1;14)(q10;p11)t(8;14)(q24;q32).
Jumping translocation of chromosome 1q
209
were applied according to the manufacturers’ guide. Fluorescence images were captured with a Zeiss Axioplan2 epifluorescence microscope and analyzed by ISIS software (MetaSystems, Altlussheim, Germany).
Results Conventional cytogenetic analysis revealed the following karyotype: 46,XY,þder(1),t(8;14)(q24;q32),21[12]/47,XY,þ i(1)(q10),t(8;14)(q24;q32)[4]/46,XY,þder(1),t(8;14))(q24;q32), 14[4]. The specific translocation t(8;14) could be detected in all analyzed metaphases, along with secondary aberrations. Three cell lines were distinguished. In the first, a derivative chromosome 1 was detected, while chromosome 21 was missing. The second cell line carried a supernumerary isochromosome of 1q (Fig. 1A). In the third cell line, a structurally rearranged chromosome 1 and monosomy of chromosome 14 were observed. FISH analysis with IGH/MYC, CEP8 fusion probes resulted in two fusion signals in 85% of 200 interphase cells analyzed, confirming an t(8;14)(q24;q32) (Fig. 1B). FISH analysis using subtelomeric probes for 1pter and 1qter showed trisomy of 1qter in 55% of 300 interphase cells analyzed. Tetrasomy of 1qter could be detected in 2% of the cells, confirming the different involvement of 1q in the observed secondary rearrangements. mFISH analysis confirmed the presence of the t(8;14) in all three cell lines and isochromosome 1q in the second one. By means of this method, we could clarify that der(1) detected in the first cell line was a result of a translocation between chromosome 1q and 21p (Fig. 1A). Moreover, in the third cell line, a complex translocation was detected in which 1q had been translocated to the derivative chromosome 14 originating from the t(8;14) (Fig. 1C). On the basis of cytogenetic and FISH analyses, the final karyotype was described as follows: 46,XY,der(21)t(1;21) (q10;p10),t(8;14)(q24;q32)[12]/47,XY,þi(1)(q10),t(8;14)(q24; q32)[4]/46,XY,der(14)t(1;14)(q10;p11)t(8;14)(q24;q32)[4].
Discussion Structural rearrangements involving the long arm of chromosome 1 are frequently found in MM, MDS and myeloproliferative Table 1
disorders. The most common changes are duplications and translocations of 1q to other chromosomes. Unbalanced translocations of 1q result in the formation of a derivative chromosome containing an extra copy of 1q. Genetic instability of chromosome 1 may be induced by cytotoxic chemotherapy or may be the consequence of disease progression (6, 7). It has been suggested that viral infection, immunodeficiency, DNA hypomethylation and chromosomal instability could lead to 1q trisomy as well (8). The extra copy of 1q is thought to give a proliferative advantage to the tumor cells and therefore, it can be considered as a secondary aberration associated with the basic neoplastic event (9). Acquired jumping translocations are rare secondary aberrations appearing most often in acute lymphoproliferative disorders such as Burkitt lymphoma or leukemia where 1q abnormalities follow the t(8;14)(q24;q32) and usually indicate a poor prognosis. To date, six cases of JT of 1q have been published in Burkitt leukemia/lymphoma (Table 1). The main breakpoints on the donor 1q can be at q11, q12, and q21. The most frequent recipients are chromosomes 13, 14, and 18. Most patients experienced aggressive disease or early relapse (5,10e13). In the present case of Burkitt leukemia, a t(8;14) (q24;q32) was found in every cell line of the blast population. This specific translocation was accompanied by different 1q abnormalities in addition to two normal chromosomes 1, resulting in trisomy or tetrasomy of 1q. In one of the three cell lines, isochromosome 1q appeared as an alternative form of tetrasomy 1q. In the other two cell lines, JT of 1q to chromosome 21 and der(14) was identified, resulting in trisomy 1q. In the case of the der(14), the basic rearrangement was t(8;14), and the der(14) seemed to be the recipient chromosome in the JT. The same complex translocation in BL has been published only in one other case in the literature (5). Molecular cytogenetic methods such as mFISH proved to be a valuable technique to complete the routine conventional cytogenetics and interphase FISH in clarifying complex karyotype abnormalities. Even though all secondary aberrations detected in each cell line reflect the progression of the disease, in the case presented here, they were associated with a favorable clinical course and outcome. We hypothesize that the number and the type of partner chromosomes, the breakpoints involved in the rearrangements, and/or the presence of additional aberrations may have a prognostic impact, but confirmation of this assumption will require further cases to be studied.
Summary of reported jumping translocations in Burkitt leukemia/lymphoma
Patient no.
Reference
Burkitt leukemia/ lymphoma
Event-free survival (mo)
1
Fitzgerald and Morris (10)
Leukemia
9
2 3
Whang-Peng et al. (11) Shikano et al. (12)
Lymphoma Lymphoma
4 8
4 5 6
Leukemia Leukemia Lymphoma
2
Seghezzi et al. (13) Manola et al. (5)
7
Present case
Leukemia
Stem line
Jumping translocation
46,XX,del(7)(q22q32), t(8;14)(q24.1;q32) 46,XY,t(8;14) 46,XY,del(7),t(8;14)
1q11 1q21 1q21
6
46,XY,t(8;14)(q24;q32) 46,XX,t(8;14)(q24;q32) 46,XY,t(8;14)(q24;q32)
1q21 1q11 1q12
90
46,XY,t(8;14)(q24;q32)
1q10
7q, 11q, 13q, 15q, 18q, 21p, Xq 4q, 19q 1q, 11p, 13p, 13q, 14q, 17q, 18p, 18q, Yp1 1q, 13p, 14p 13q, 14p, 15p, 22p 13q34, 21q22, 14p11, 18q22 1q10, 14p11, 21p10
210
B. Bessenyei et al.
Acknowledgments This work was supported by the Hungarian Scientific Research Fund (OTKA) project K49292, by the grants ETT 443-01 and T.I.O.P.4.2.1.B, and by the Leukemic Children and Hope for the Leukemic Children foundations.
References 1. Berger R, Bernard OA. Jumping translocations. Genes Chromosomes Cancer 2007;46:717e723. 2. Bench AJ, Cross NCP, Huntly BJP, et al. Myeloproliferative disorders. Best Pract Res Clinic Haematol 2001;14:531e551. 3. Hanamura I, Stewart JP, Huang Z, et al. Frequent gain of chromosome band 1q21 in plasma cell dyscrasias detected by fluorescence in situ hybridization: incidence increases from MGUS to relapsed myeloma and is related to prognosis and disease progression following tandem stem cell transplantation. Blood 2006;108:1724e1732. 4. Fonatsch C, Haase D, Freund M, et al. Partial trisomy 1q. A nonrandom primary chromosomal abnormality in myelodysplastic syndromes. Cancer Genet Cytogenet 1991;56: 243e253. 5. Manola KN, Georgakakos VN, Stavropoulou C, et al. Jumping translocations in hematological malignancies: a cytogenetic
6.
7.
8.
9.
10.
11. 12.
13.
study of five cases. Cancer Genet Cytogenet 2008;187: 85e94. Sawyer JR, Tricot G, Mattox S, et al. Jumping translocations of chromosome 1q in multiple myeloma: evidence for a mechanism involving decondensation of pericentromeric heterochromatin. Blood 1998;91:1732e1741. Almeida A, Kokalj-Vokac N, Lefrancois D, et al. Hypomethylation of classical satellite DNA and chromosome instability in lymphoblastoid cell lines. Hum Genet 1993;91:538e546. Sawyer JR, Swanson CM, Koller MA, et al. Centromeric instability of chromosome resulting in multibranched chromosomes, telomeric fusions, and "jumping translocations" of 1q in a human immunodeficiency virus-related non-Hodgkin’s lymphoma. Cancer 1995;76:1238e1244. Morris CM, Fitzgerald PH, Neville MA, et al. Does multisomy of chromosome 1q confer a proliferative advantage in B-cell acute lymphoblastic leukemia? Cancer 1984;54:48e53. Fitzgerald PH, Morris CM. Telomeric association of chromosomes in B-cell lymphoid leukemia. Hum Genet 1984;67: 385e390. Whang-Peng J, Lee EC, Sieverts H, et al. Burkitt’s lymphoma in AIDS: cytogenetic study. Blood 1984;63:818e822. Shikano T, Arioka H, Kobayashi R, et al. Jumping translocations of 1q in Burkitt lymphoma and acute nonlymphocytic leukemia. Cancer Genet Cytogenet 1993;71:22e26. Seghezzi L, Addis P, Giglio S, et al. Jumping translocations in acute lymphoblastic leukemia. Cancer Genet Cytogenet 1995; 80:80e81.
BRIEF COMMUNICATION
Jumping translocation of chromosome 1q associated with good clinical outcome in a case of Burkitt leukemia Beata Bessenyei a,*, Aniko Ujfalusi a, Erzsebet Balogh a, Eva Olah a, Istvan Szegedi b, Csongor Kiss b a
Clinical Genetic Center, Department of Pediatrics, University of Debrecen Medical and Health Science Center, Debrecen, Hungary; b Division of Hematology, Department of Pediatrics, University of Debrecen Medical and Health Science Center, Debrecen, Hungary Acquired jumping translocations (JTs) are rare secondary aberrations occurring in various hematological malignancies. In Burkitt lymphoma/leukemia (BL) chromosome 1q abnormalities such as partial or whole arm duplications/translocations are frequently associated with the diseasespecific t(8;14)(q24;q32). JTs of 1q are considered to have a bad prognostic impact in BL. We report clinical, conventional and molecular cytogenetic findings of a 12-year-old boy who presented with BL. In addition to the primary aberration, t(8;14)(q24;q32), JT of 1q onto chromosomes 21 and der(14) as well as the formation of isochromosome 1q could be detected in his bone marrow sample. Despite the expected poor prognostic outcome of these aberrations, the patient has been experiencing an event free survival of 7.5 years at the time of the present report, reflecting the excellent clinical outcome of the disease. Keywords Jumping translocation, 1q, Burkitt leukemia, mFISH ª 2011 Elsevier Inc. All rights reserved.
Jumping translocations (JTs) are rare cytogenetic aberrations involving a donor chromosome arm or segment that is fused to two or more different recipient chromosomes in different cell lines of the same patient (1). They may be constitutional or acquired rearrangements and occur in various pathologic conditions. JTs are rare aberrations in hematological malignancies, but they have been described in various diseases including acute myeloid leukemia (AML) M1 and M5, BCR/ABL positive acute lymphoblastic leukemia (ALL), myelodysplastic syndrome (MDS), multiple myeloma (MM) and Burkitt lymphoma/leukemia (BL) (2e5). An extra copy of chromosome 1q is a common secondary aberration in Burkitt leukemia associated with L3 morphology of lymphoblasts, mature B-cell immunophenotype (sIg) and with the specific translocation, t(8;14)(q24;q32) or its variants, t(8;22)(q24;q11) and t(2;8)(p12;q24). An extra copy of 1q usually originates from a translocated unbalanced derivate chromosome, an isochromosome or a jumping translocation. JT of 1q have usually been reported to be Received February 18, 2010; received in revised form September 2, 2010; accepted October 27, 2010. * Corresponding author. E-mail address: [email protected] 2210-7762/$ - see front matter ª 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.cancergencyto.2010.10.005
associated with a poor clinical outcome (1). Hereby, we present a case with a JT of 1q associated with a good prognosis in a case of Burkitt leukemia with atypical late preB cell immunophenotype and t(8;14)(q24;q32) translocation.
Materials and methods Patient A 12-year-old boy sought care for weakness, headache, fever, and skin suffusions. At admission, peripheral blood tests revealed a white blood cell count of 27.6 109/L, hemoglobin of 112 g/L, and platelet count of 19 109/L. A bone marrow aspirate showed 50% blasts with Frenche AmericaneBritish L3 morphology. Immunophenotyping of the blasts by flow cytometry identified atypical, late pre-B-cell phenotype with CD10, CD19, CD45, CD71, cyCD79a, and cy IgM antigen expression. Blasts were negative for surface immunoglobulin light chains. Lumbar puncture was performed, and the results revealed no evidence of atypical cells in the cerebrospinal fluid. Cytogenetic analysis showed a t(8;14)(q24;q32) and a jumping translocation of 1q. Based on the morphology and the immunophenotype of the blasts
208 along with cytogenetic data, a diagnosis of Burkitt leukemia was made. Cytostatic therapy according to the non-Hodgkin €nster group trial (NHL BFM lymphoma Berlin-Frankfurt-Mu 95, branch II, R4) was introduced. The patient experienced complete hematologic and cytogenetic remission, which was maintained for 7.5 years after the diagnosis.
Cytogenetic analysis Conventional cytogenetic analysis was performed on bone marrow leukocytes at the time of diagnosis after a 24-hourlong culture by standard techniques and was evaluated
B. Bessenyei et al. by G banding. Twenty metaphases were analyzed and the karyotype was described according to the International System for Human Cytogenetic Nomenclature (ISCN, 2009).
Fluorescence in situ hybridization (FISH) analysis FISH studies were performed on bone marrow cytogenetic specimens at diagnosis using the following commercial DNA probes: LSI IGH/MYC, CEP8 (Abbott Molecular, Des Plaines, IL); 1pter and 1qter subtelomere specific probes (Cytocell, Cambridge, UK); 24XCyte multicolor FISH (mFISH) probe kit (MetaSystems, Altlussheim, Germany). All probes
Figure 1 (A) Partial G-banded and multicolor fluorescence in situ hybridization (mFISH) karyograms of two cells showing der(1) and i(1)(q10) besides the two normal chromosomes 1. mFISH clarified that der(1) resulted from a t(1;21)(q10;p10) and confirmed the i(1)(q10). Arrows indicate the abnormal chromosomes. (B) Interphase FISH using IGH/MYC probes shows one normal IGH (green) signal, one normal MYC (orange) signal, and two fusion signals indicating a t(8;14)(q24;q32). (C) mFISH karyogram of the third cell line showing 46,XY,der(14)t(1;14)(q10;p11)t(8;14)(q24;q32).
Jumping translocation of chromosome 1q
209
were applied according to the manufacturers’ guide. Fluorescence images were captured with a Zeiss Axioplan2 epifluorescence microscope and analyzed by ISIS software (MetaSystems, Altlussheim, Germany).
Results Conventional cytogenetic analysis revealed the following karyotype: 46,XY,þder(1),t(8;14)(q24;q32),21[12]/47,XY,þ i(1)(q10),t(8;14)(q24;q32)[4]/46,XY,þder(1),t(8;14))(q24;q32), 14[4]. The specific translocation t(8;14) could be detected in all analyzed metaphases, along with secondary aberrations. Three cell lines were distinguished. In the first, a derivative chromosome 1 was detected, while chromosome 21 was missing. The second cell line carried a supernumerary isochromosome of 1q (Fig. 1A). In the third cell line, a structurally rearranged chromosome 1 and monosomy of chromosome 14 were observed. FISH analysis with IGH/MYC, CEP8 fusion probes resulted in two fusion signals in 85% of 200 interphase cells analyzed, confirming an t(8;14)(q24;q32) (Fig. 1B). FISH analysis using subtelomeric probes for 1pter and 1qter showed trisomy of 1qter in 55% of 300 interphase cells analyzed. Tetrasomy of 1qter could be detected in 2% of the cells, confirming the different involvement of 1q in the observed secondary rearrangements. mFISH analysis confirmed the presence of the t(8;14) in all three cell lines and isochromosome 1q in the second one. By means of this method, we could clarify that der(1) detected in the first cell line was a result of a translocation between chromosome 1q and 21p (Fig. 1A). Moreover, in the third cell line, a complex translocation was detected in which 1q had been translocated to the derivative chromosome 14 originating from the t(8;14) (Fig. 1C). On the basis of cytogenetic and FISH analyses, the final karyotype was described as follows: 46,XY,der(21)t(1;21) (q10;p10),t(8;14)(q24;q32)[12]/47,XY,þi(1)(q10),t(8;14)(q24; q32)[4]/46,XY,der(14)t(1;14)(q10;p11)t(8;14)(q24;q32)[4].
Discussion Structural rearrangements involving the long arm of chromosome 1 are frequently found in MM, MDS and myeloproliferative Table 1
disorders. The most common changes are duplications and translocations of 1q to other chromosomes. Unbalanced translocations of 1q result in the formation of a derivative chromosome containing an extra copy of 1q. Genetic instability of chromosome 1 may be induced by cytotoxic chemotherapy or may be the consequence of disease progression (6, 7). It has been suggested that viral infection, immunodeficiency, DNA hypomethylation and chromosomal instability could lead to 1q trisomy as well (8). The extra copy of 1q is thought to give a proliferative advantage to the tumor cells and therefore, it can be considered as a secondary aberration associated with the basic neoplastic event (9). Acquired jumping translocations are rare secondary aberrations appearing most often in acute lymphoproliferative disorders such as Burkitt lymphoma or leukemia where 1q abnormalities follow the t(8;14)(q24;q32) and usually indicate a poor prognosis. To date, six cases of JT of 1q have been published in Burkitt leukemia/lymphoma (Table 1). The main breakpoints on the donor 1q can be at q11, q12, and q21. The most frequent recipients are chromosomes 13, 14, and 18. Most patients experienced aggressive disease or early relapse (5,10e13). In the present case of Burkitt leukemia, a t(8;14) (q24;q32) was found in every cell line of the blast population. This specific translocation was accompanied by different 1q abnormalities in addition to two normal chromosomes 1, resulting in trisomy or tetrasomy of 1q. In one of the three cell lines, isochromosome 1q appeared as an alternative form of tetrasomy 1q. In the other two cell lines, JT of 1q to chromosome 21 and der(14) was identified, resulting in trisomy 1q. In the case of the der(14), the basic rearrangement was t(8;14), and the der(14) seemed to be the recipient chromosome in the JT. The same complex translocation in BL has been published only in one other case in the literature (5). Molecular cytogenetic methods such as mFISH proved to be a valuable technique to complete the routine conventional cytogenetics and interphase FISH in clarifying complex karyotype abnormalities. Even though all secondary aberrations detected in each cell line reflect the progression of the disease, in the case presented here, they were associated with a favorable clinical course and outcome. We hypothesize that the number and the type of partner chromosomes, the breakpoints involved in the rearrangements, and/or the presence of additional aberrations may have a prognostic impact, but confirmation of this assumption will require further cases to be studied.
Summary of reported jumping translocations in Burkitt leukemia/lymphoma
Patient no.
Reference
Burkitt leukemia/ lymphoma
Event-free survival (mo)
1
Fitzgerald and Morris (10)
Leukemia
9
2 3
Whang-Peng et al. (11) Shikano et al. (12)
Lymphoma Lymphoma
4 8
4 5 6
Leukemia Leukemia Lymphoma
2
Seghezzi et al. (13) Manola et al. (5)
7
Present case
Leukemia
Stem line
Jumping translocation
46,XX,del(7)(q22q32), t(8;14)(q24.1;q32) 46,XY,t(8;14) 46,XY,del(7),t(8;14)
1q11 1q21 1q21
6
46,XY,t(8;14)(q24;q32) 46,XX,t(8;14)(q24;q32) 46,XY,t(8;14)(q24;q32)
1q21 1q11 1q12
90
46,XY,t(8;14)(q24;q32)
1q10
7q, 11q, 13q, 15q, 18q, 21p, Xq 4q, 19q 1q, 11p, 13p, 13q, 14q, 17q, 18p, 18q, Yp1 1q, 13p, 14p 13q, 14p, 15p, 22p 13q34, 21q22, 14p11, 18q22 1q10, 14p11, 21p10
210
B. Bessenyei et al.
Acknowledgments This work was supported by the Hungarian Scientific Research Fund (OTKA) project K49292, by the grants ETT 443-01 and T.I.O.P.4.2.1.B, and by the Leukemic Children and Hope for the Leukemic Children foundations.
References 1. Berger R, Bernard OA. Jumping translocations. Genes Chromosomes Cancer 2007;46:717e723. 2. Bench AJ, Cross NCP, Huntly BJP, et al. Myeloproliferative disorders. Best Pract Res Clinic Haematol 2001;14:531e551. 3. Hanamura I, Stewart JP, Huang Z, et al. Frequent gain of chromosome band 1q21 in plasma cell dyscrasias detected by fluorescence in situ hybridization: incidence increases from MGUS to relapsed myeloma and is related to prognosis and disease progression following tandem stem cell transplantation. Blood 2006;108:1724e1732. 4. Fonatsch C, Haase D, Freund M, et al. Partial trisomy 1q. A nonrandom primary chromosomal abnormality in myelodysplastic syndromes. Cancer Genet Cytogenet 1991;56: 243e253. 5. Manola KN, Georgakakos VN, Stavropoulou C, et al. Jumping translocations in hematological malignancies: a cytogenetic
6.
7.
8.
9.
10.
11. 12.
13.
study of five cases. Cancer Genet Cytogenet 2008;187: 85e94. Sawyer JR, Tricot G, Mattox S, et al. Jumping translocations of chromosome 1q in multiple myeloma: evidence for a mechanism involving decondensation of pericentromeric heterochromatin. Blood 1998;91:1732e1741. Almeida A, Kokalj-Vokac N, Lefrancois D, et al. Hypomethylation of classical satellite DNA and chromosome instability in lymphoblastoid cell lines. Hum Genet 1993;91:538e546. Sawyer JR, Swanson CM, Koller MA, et al. Centromeric instability of chromosome resulting in multibranched chromosomes, telomeric fusions, and "jumping translocations" of 1q in a human immunodeficiency virus-related non-Hodgkin’s lymphoma. Cancer 1995;76:1238e1244. Morris CM, Fitzgerald PH, Neville MA, et al. Does multisomy of chromosome 1q confer a proliferative advantage in B-cell acute lymphoblastic leukemia? Cancer 1984;54:48e53. Fitzgerald PH, Morris CM. Telomeric association of chromosomes in B-cell lymphoid leukemia. Hum Genet 1984;67: 385e390. Whang-Peng J, Lee EC, Sieverts H, et al. Burkitt’s lymphoma in AIDS: cytogenetic study. Blood 1984;63:818e822. Shikano T, Arioka H, Kobayashi R, et al. Jumping translocations of 1q in Burkitt lymphoma and acute nonlymphocytic leukemia. Cancer Genet Cytogenet 1993;71:22e26. Seghezzi L, Addis P, Giglio S, et al. Jumping translocations in acute lymphoblastic leukemia. Cancer Genet Cytogenet 1995; 80:80e81.