HereditasVolume 84, Issue 2 p. 231-232 Open Access Philadelphia chromosome in acute lymphocytic leukaemia Preben Philip, Corresponding Author Preben Philip*Division of Haematology, Department of Medicine A Rigshospitalet Blegdamsvej 9 DK-2100 Copenhagen Ø, DenmarkSearch for more papers by this authorNicoleMuller -Berat, NicoleMuller -BeratSearch for more papers by this authorWen-Aage Killmann, Wen-Aage KillmannSearch for more papers by this author Preben Philip, Corresponding Author Preben Philip*Division of Haematology, Department of Medicine A Rigshospitalet Blegdamsvej 9 DK-2100 Copenhagen Ø, DenmarkSearch for more papers by this authorNicoleMuller -Berat, NicoleMuller -BeratSearch for more papers by this authorWen-Aage Killmann, Wen-Aage KillmannSearch for more papers by this author First published: February 1977 https://doi.org/10.1111/j.1601-5223.1977.tb01399.xCitations: 3AboutPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume84, Issue2February 1977Pages 231-232 RelatedInformation

HereditasVolume 93, Issue 1 p. 185-185 Open Access 14q+-A consistent marker of plasma cell leukaemia Preben Philip, Corresponding Author Preben Philip Division of Haematology Department of Medicine A Rigshospitalet Blegdamsvej 9 DK-2100 Copenhagen, DenmarkDepartment of Medicine A, Division of Haematology, Rigshospitalet, State University Hospital of Copenhagen, DenmarkSearch for more papers by this authorSven-Aage Killman, Sven-Aage Killman Division of Haematology Department of Medicine A Rigshospitalet Blegdamsvej 9 DK-2100 Copenhagen, DenmarkSearch for more papers by this author Preben Philip, Corresponding Author Preben Philip Division of Haematology Department of Medicine A Rigshospitalet Blegdamsvej 9 DK-2100 Copenhagen, DenmarkDepartment of Medicine A, Division of Haematology, Rigshospitalet, State University Hospital of Copenhagen, DenmarkSearch for more papers by this authorSven-Aage Killman, Sven-Aage Killman Division of Haematology Department of Medicine A Rigshospitalet Blegdamsvej 9 DK-2100 Copenhagen, DenmarkSearch for more papers by this author First published: September 1980 https://doi.org/10.1111/j.1601-5223.1980.tb01061.xCitations: 1AboutPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume93, Issue1September 1980Pages 185-185 ReferencesRelatedInformation

HereditasVolume 89, Issue 2 p. 268-268 Open Access Burkitt type 14 + marker chromosome in B-cell type acute lymphocytic leukaemia Preben Philip, Corresponding Author Department of Medicine A, Rigshospitalet, State University Hospital of Copenhagen, Denmark Department of Medicine C, Gentofte Hospital, University Hospital of Copenhagen, Denmark Human Genetics Laboratory, University of Amsterdam, Holland and Roswell Park Memorial Institute, Buffalo, New York, U.S.A.*Division of Haematology Department of Medicine A Rigshospitalet Blegdamsvej 9 DK-2100 Copenhagen, DenmarkSearch for more papers by this authorRosalyn M. Slater, Department of Medicine A, Rigshospitalet, State University Hospital of Copenhagen, Denmark Department of Medicine C, Gentofte Hospital, University Hospital of Copenhagen, Denmark Human Genetics Laboratory, University of Amsterdam, Holland and Roswell Park Memorial Institute, Buffalo, New York, U.S.A.Search for more papers by this authorAvery A. Sandberg, Department of Medicine A, Rigshospitalet, State University Hospital of Copenhagen, Denmark Department of Medicine C, Gentofte Hospital, University Hospital of Copenhagen, Denmark Human Genetics Laboratory, University of Amsterdam, Holland and Roswell Park Memorial Institute, Buffalo, New York, U.S.A.Search for more papers by this author Preben Philip, Corresponding Author Department of Medicine A, Rigshospitalet, State University Hospital of Copenhagen, Denmark Department of Medicine C, Gentofte Hospital, University Hospital of Copenhagen, Denmark Human Genetics Laboratory, University of Amsterdam, Holland and Roswell Park Memorial Institute, Buffalo, New York, U.S.A.*Division of Haematology Department of Medicine A Rigshospitalet Blegdamsvej 9 DK-2100 Copenhagen, DenmarkSearch for more papers by this authorRosalyn M. Slater, Department of Medicine A, Rigshospitalet, State University Hospital of Copenhagen, Denmark Department of Medicine C, Gentofte Hospital, University Hospital of Copenhagen, Denmark Human Genetics Laboratory, University of Amsterdam, Holland and Roswell Park Memorial Institute, Buffalo, New York, U.S.A.Search for more papers by this authorAvery A. Sandberg, Department of Medicine A, Rigshospitalet, State University Hospital of Copenhagen, Denmark Department of Medicine C, Gentofte Hospital, University Hospital of Copenhagen, Denmark Human Genetics Laboratory, University of Amsterdam, Holland and Roswell Park Memorial Institute, Buffalo, New York, U.S.A.Search for more papers by this author First published: December 1978 https://doi.org/10.1111/j.1601-5223.1978.tb01285.xCitations: 2AboutPDF ToolsExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume89, Issue2December 1978Pages 268-268 ReferencesRelatedInformation

6 cases of AML with a supernumerary chromosome 8 as the only aberration in practically all bone marrow mitoses and 10 cases with a normal chromosome composition of the marrow cells were investigated in order to evaluate the possible influence of trisomy 8 on some clinical and cytokinetic parameters. No significant differences between the groups were found. In our laboratory a supernumerary chromosome 8 is present in 36% of AML cases with chromosomal aberrations.

European Journal of HaematologyVolume 83, Issue 2 p. 156-158 Danish CLL2-Study revisited: FISH on a cohort with a 20-yr follow-up confirms the validity of the hierarchical model of genomic aberrations in chronic lymphocytic leukaemia Christian Geisler, Christian Geisler Department of Haematology, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorJesper Jurlander, Jesper Jurlander Department of Haematology, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorLars Bullinger, Lars Bullinger The Chromosome Laboratory, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorSandrine Sander, Sandrine Sander The Chromosome Laboratory, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorPeter Brown, Peter Brown Department of Haematology, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorAxel Benner, Axel Benner The Chromosome Laboratory, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorPreben Philip, Preben Philip Department of Haematology, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorHartmut Döhner, Hartmut Döhner The Chromosome Laboratory, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorStephan Stilgenbauer, Stephan Stilgenbauer The Chromosome Laboratory, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorfor the Danish CLL-2 study group, for the Danish CLL-2 study group Department of Haematology, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this author Christian Geisler, Christian Geisler Department of Haematology, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorJesper Jurlander, Jesper Jurlander Department of Haematology, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorLars Bullinger, Lars Bullinger The Chromosome Laboratory, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorSandrine Sander, Sandrine Sander The Chromosome Laboratory, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorPeter Brown, Peter Brown Department of Haematology, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorAxel Benner, Axel Benner The Chromosome Laboratory, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorPreben Philip, Preben Philip Department of Haematology, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorHartmut Döhner, Hartmut Döhner The Chromosome Laboratory, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorStephan Stilgenbauer, Stephan Stilgenbauer The Chromosome Laboratory, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this authorfor the Danish CLL-2 study group, for the Danish CLL-2 study group Department of Haematology, Rigshospitalet, Copenhagen, DenmarkSearch for more papers by this author First published: 02 July 2009 https://doi.org/10.1111/j.1600-0609.2009.01258.xCitations: 5 Christian Geisler, Deptartment of Haematology, L4042, Rigshospitalet, 9 Blegdamsvej, DK 2100 Copenhagen, Denmark. Tel: +45 35451146; Fax: +45 35454841; e-mail: christian.geisler@rh.regionh.dk Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume83, Issue2August 2009Pages 156-158 RelatedInformation

During the period from 1995 to 1997, we studied 19 new cases of therapy-related myelodysplasia (t-MDS) and acute myeloid leukemia (t-AML), extending our series to 180 consecutive cases: 123 patients with t-MDS and 57 patients with t-AML. Cytogenetically unrelated clones were observed in 13 patients: I I patients with two unrelated clones, one patient with three unrelated clones, and one patient with four unrelated clones. Twelve cases of unrelated clones presented as t-MDS, whereas only one case presented as overt t-AML. Partial or complete deletions of the long arms or monosomy for chromosome 5 or chromosome 7, which are characteristic of t-MDS and t-AML, were observed in both unrelated clones in four patients and in one unrelated clone only in six patients, whereas three patients showed aberrations in both clones that were uncharacteristic of t-MDS or t-AML, Three different interpretations of the origin and significance of cytogenetically unrelated clones in t-MDS and t-AML are presented, although the disease is still considered to be monoclonal. First, patients with different defects of the long arm of chromosome 5 or chromosome 7 in Mo unrelated clones often seem to have acquired these aberrations as independent events. For this reason, it is possible that they may play an important role in leukemic transformation, for instance, by activating or potentiating the effect of a genetic change that is present in all cells but not disclosed as a visible chromosome abnormality. In cases with involvement of other chromosomes, unrelated clones sometimes develop by cytogenetic change in only a subclone of cells, indicating that they play a role only in tumor progression. Finally, unrelated clones in t-MDS and t-AML may represent MO different monoclonal diseases: the primary tumor and t-MDS. This view is supported by the significant excess of unrelated clones observed in t-MDS following multiple myeloma (4 in 13 cases) compared with other diseases (9 in 167 cases; P = 0.02), and by results from a case with a balanced translocation that is highly characteristic of non-Hodgkin's lymphoma in one clone and a t-MDS-associated deletion of the long arm of chromosome 5 in another. Genes Chromosomes Cancer 23.337-349, 1998. (C) 1998 Wiley-Liss, Inc.

Of 560 consecutive, newly diagnosed untreated patients with B CLL submitted for chromosome study, G-banded karyotypes could be obtained in 480 cases (86%). Of these, 345 (72%) had normal karyotypes and 135 (28%) had clonal chromosome abnormalities: trisomy 12 (+12) was found in 40 cases, 20 as +12 alone (+12single), 20 as +12 with additional abnormalities (+12complex). Other frequent findings included abnormalities of 14q, chromosome 17, 13q and 6q. The immunophenotype was typical for CLL in 358 patients (CD5+, Slg(weak), mainly FMC7-) and atypical for CLL in 122 patients (25%) (CD5-, or Slg(strong) or FMC7+). Chromosome abnormalities were found significantly more often in patients with atypical (48%) than in patients with typical CLL phenotype (22%) (P < 0.00005). Also +12complex, 14q+, del6q, and abnormalities of chromosome 17 were significantly more frequent in patients with atypical CLL phenotype, whereas +12single was found equally often in patients with typical and atypical CLL phenotype. The cytomorphology of most of the +12 patients was that of classical CLL irrespective of phenotype. In univariate survival analysis the following cytogenetic findings were significantly correlated to a poor prognosis: chromosome 17 abnormalities, 14q+, an abnormal karyotype, +12complex, more than one cytogenetic event, and the relative number of abnormal mitoses. In multivariate survival analysis chromosome 17 abnormalities were the only cytogenetic findings with independent prognostic value irrespective of immunophenotype. We conclude that in patients with typical CLL immunophenotype, chromosome abnormalities are somewhat less frequent at the time of diagnosis than hitherto believed. +12single is compatible with classical CLL, and has no prognostic influence whereas chromosome 17 abnormalities signify a poor prognosis. In patients with an atypical CLL immunophenotype, chromosome abnormalities including +12complex, 14q+, del 6q and chromosome 17 are found in about 50% of the patients, and in particular chromosome 17 abnormalities suggest a poor prognosis.

Chronic neutrophil leukaemia (CNL) is a rare myeloproliferative disorder predominantly reported in elderly patients. We present a 15‐year‐old girl and a 25‐year‐old male with CNL. Clonal cytogenetic abnormalities were detected in both patients. One showed trisomy 21 evolving into tetrasomy 21. The second patient showed a unique chromosome aberration during blast crisis: t(2;2)(q32;p24). Both patients were successfully treated with allogeneic bone marrow transplantation (BMT). CNL should also be considered as a differential diagnosis in adolescence and young adulthood. BMT represents a potentially curative treatment option in such patients.

Development of myelodysplasia (MDS) with subsequent progression to acute myeloid leukemia (AML) is an example of the multistep process of malignant transformation in which each step often relates to genetic abnormalities that can be directly seen as chromosomal aberrations. Therapy-related MDS and AML (t-MDS and t-AML) may serve as an ideal model for a study of the genetic evolution of MDS and AML because chromosomal abnormalities are observed in most cases and because the disease is often diagnosed early due to a close patient follow-up. The cytogenetic characteristics at diagnosis were studied in 137 consecutive cases of t-MDS and t-AML, including 22 new cases, and correlated with the clinical characteristics and the course of the disease. Balanced translocations to chromosome bands 11q23 and 21q22 represent primary steps in pathways leading directly to overt t-AML. Specific chromosomal deletions or losses, on the other hand, represent primary or secondary events in alternative pathways leading to t-MDS with potential for subsequent transformation to overt t-AML. Loss of a whole chromosome 7 (-7) or deletion of its long arm (7q-) and deletion of the long arm of a chromosome 5 (5q-) were the most frequent primary abnormalities significantly related to t-MDS. Loss of a whole chromosome 5 (-5) was also a primary event, but surprisingly, was observed equally in t-MDS and in t-AML. Deletion of chromosome 13, including bands q13q14, was another less common primary aberration of t- MDS. Except for -7 and del(13q), these primary aberrations were most often observed together with secondary abnormalities. These included balanced aberrations involving band 3q26 and various deletions of chromosome 3, a gain of a whole chromosome 8, deletions of the short arm or loss of chromosomes 12 and 17, loss of a whole chromosome 18, and deletions of the short arm of chromosome 21. Deletions or loss or chromosomes 5 and 7 were significantly associated with previous therapy with alkylating agents (P = .002), and balanced translocations to chromosome bands 3q26, 11q23, and 21q22 were significantly associated with previous therapy with drugs targeting DNA-topoisomerase II (P < .00005). Other characteristic aberrations were not related to any specific type of therapy. The molecular changes believed to contribute to the development of t-MDS and t-AML have been identified for many of these chromosomal abnormalities.

For more than 20 years the many aspects of t-MDS and t-AML, including risk factors incidence and chromosome characteristics: have been evaluated in numerous studies, as reviewed extensively elsewhere [1–7]. The risk has primarily been related to previous therapy with the alkylating agents, but more recently also to therapy with the epipodophyllotoxins. In a few studies high voltage radiotherapy has been shown to play a minor role, in other studies it was not a significant risk factor. Risk estimates have shown great variation from study to study, probably due to differences in patient age and treatment intensity. In addition variation in ascertainment of cases may also have played a role, as cases of t-MDS may easily have been overlooked in studies where cytogenetic screening was not performed in all patients developing refractory, unexplained cytopenia. Since the first report in 1977 [8], however, a more consistent finding in t-MDS and t-AML after therapy with alkylating agents has been the loss of whole chromosomes no. 5 or no. 7, or of various parts of the long arm of these two chromosomes. Recently, rearrangements of the long arm of chromosome no. 11 were reported as characteristic of leukemias following therapy with the epipodophyllotoxins [9,10]. Subsequently, specific balanced translocations involving bands 11q23 and 21q22 were shown to be significantly associated not only with previous therapy with the epipodophyllotoxins but also with other cytostatic drugs targeting at DNA-topoisomerase II such as the anthracyclines [11,12].

Translocation (3;21)(q26;q22) has been observed only rarely in de novo myelodysplasia (MDS) and de novo acute myeloid leukemia (AML), but, including the two new cases in the present study, the aberration has now been identified in at least 10 cases of t-MDS or t-AML. All these 10 patients had previously received alkylating agents, in nine patients combined with a drug targeting at DNA-topoisomerase II (doxorubicin in eight cases). Eight of the ten patients presented with t-MDS. A further 20 patients with various myeloproliferative disorders and an identical t(3;21) have been reported. In these cases, t(3;21) was not related to any specific type of previous therapy but was associated with transformation from chronic stage disease to overt AML.

Short-term liquid marrow culture (STLMC) is a potential source for autografting in leukemia. In a preclinical setting, including candidates for autologous marrow transplantation, we have studied STLMC supported by a selected mixture of clinical available recombinant human haematopoietic growth factors. STLMC of leukemic marrow cells were prospectively performed to evaluate the purging effect. Bone marrow cells cultured and supported by the selected mixture of rhIL-3/rhGM-CSF/rhEpo revealed an increased number of day 10-12 cultured cells, parallelled by an increased proliferation rate when compared to unstimulated cultures. The median number of myeloid progenitors recognized as day 7 and day 14 granulocyte-macrophage colony-forming units (day 7/14 GM-CFU) was significantly increased in the supported STLMC to 145/305 from 105/115 per ml culture (n = 7, p < 0.01). Further addition of rhKL did not enhance the numbers of day 7 or day 14 GM-CFUs per ml culture. In no instance was the number of clonogenic cells at the end of culture greater than the input day 0, except in cultures of purified CD34-positive marrow progenitors which resulted in an expansion of late myeloid progenitors. Cytokine-supported cultures of leukemic marrow cells from acute myeloid (n = 14) and lymphoblastic (n = 7) leukemia patients were established at the time of diagnosis. In the supported cultures, the cell number increased for myeloblast but was unchanged for lymphoblast leukemic marrow cells compared to non-supported cultures. Immunophenotypic and cytogenetic studies of selected leukemic cell samples identified unchanged myeloid or slightly reduced frequencies of lymphoblastic leukemic cells at the end of culture. This preclinical study supports the idea that the addition of a mixture of clinical available haemopoietic cytokines to STLMC increases the recovery of detectable myeloid progenitors which may enhance myeloid regeneration after autografting. No substantial selective loss of myeloid leukemic cells was found in the cytokine-supported short-term culture system.

Therapy-related acute myeloid leukemia (t-AML), often presenting as myelodysplasia (t-MDS), has become the most serious long-term complication of cancer therapy and offers a unique opportunity to study chemical leukemogenesis. Seven cohorts of patients treated for six different types of primary tumor have been followed closely for leukemic complications, and 115 consecutive patients with t-MDS or t-AML, including 45 cases from the cohorts, have been investigated cytogenetically at our institutions during the past 16 years. In patients primarily treated with alkylating agents, the risk of t-MDS and t-AML increased by approximately 1% per year from 2 to at least 8 years after start of treatment. In most cases, the disease presented as t-MDS with loss of a whole chromosome 5 or 7, or various parts of their long arms, and the leukemias were of FAB-subtypes M1, M2, or M4. In patients treated with drugs targeting at DNA-topoisomerase II, such as etoposide, doxorubicin, 4-epidoxorubicin, or mitoxantrone combined with drugs reacting directly with DNA, such as cisplatin or alkylating agents, the risk of leukemia increased much more steeply from only one year after start of therapy. These early onset cases often presented as overt leukemia of FAB-subtypes M4 or M5 with balanced translocations to chromosome bands 11q23 and 21q22, whereas later onset cases often shared characteristics with cases observed after therapy with alkylating agents alone. Both alkylation of DNA and poisoning of DNA-topoisomerase II may result in development of t-AML with different clinical and cytogenetic characteristics. There may be a synergistic leukemogenic effect between the two types of drug, and in patients with germ cell tumors treated with etoposide, cisplatin and bleomycin, reassessment suggested the risk of leukemia to increase exponentially with increasing doses of cisplatin and etoposide.

PURPOSE To report five cases of acute monocytic or myelomonocytic leukemia after chemotherapy with 4-epidoxorubicin for breast cancer and to evaluate the risk of leukemia after the use of this drug. PATIENTS AND METHODS One hundred fifty-seven patients with advanced breast cancer were randomized to either 4-epi-doxorubicin plus cisplatin or 4-epi-doxorubicin alone. An additional 203 patients were treated prospectively with 4-epi-doxorubicin alone. All were observed closely for leukemic complications. RESULTS Three patients from the randomized study developed leukemia; all were in the subgroup of 74 patients who received 4-epi-doxorubicin plus cisplatin, whereas no leukemia was observed among the remaining 83 patients in the randomized study or among the additional 203 patients who were treated prospectively with 4-epi-doxorubicin alone (P = .023, log-rank test). In the subgroup of 74 patients who were treated with 4-epi-doxorubicin plus cisplatin, the cumulative risk of leukemia was 16.0% +/- 9.9% (mean +/- SE) 33 months after the start of therapy; the relative risk was 668 (95% confidence interval [Cl], 138 to 1,953). Two other cases of acute monocytic and myelomonocytic leukemia were observed after 4-epi-doxorubicin plus alkylating agents were administered for breast cancer. Three of five cases of leukemia presented balanced translocations to chromosome band 11q23 and two, loss of a whole chromosome no. 7 or its long arm. CONCLUSIONS 4-epi-doxorubicin is leukemogenic, and the leukemias are often acute monocytic or myelomonocytic with balanced chromosome translocations to band 11q23, such as in the leukemias after therapy with the epipodophyllotoxins. Furthermore, our results suggest a synergistic effect in leukemogenesis between 4-epi-doxorubicin targeting DNA-topoisomerase II and directly genotoxic drugs such as cisplatin or alkylating agents.

Two different classes of therapy-related acute myeloid leukemia (t-AML) seem to emerge. One class follows therapy with alkylating agents, increases in frequency with age, often presents with myelodysplasia (MDS), responds poorly to chemotherapy, and shows monosomy 7(-7), monosomy 5(-5), or loss of various parts of the long arms of these chromosomes (5q- and 7q-). The other class is related to therapy with cytostatic drugs targeting at DNA-topoisomerase II, often presents with overt leukemia, responds more favorably to chemotherapy, and shows balanced chromosome aberrations, primarily translocations involving chromosome bands 11q23 and 21q22. These two classes of t-AML may have their counterparts in de-novo acute myeloid leukemia (de-novo AML).