A unique case of t(15;17) acute promyelocytic leukaemia (M3) developing into acute myeloblastic leukaemia (M1) with t(7;21) at relapse

T, Jubashi; Nagai, Kazuhiro; Miyazaki, Yasushi; Nakamura, Hideo; Matsuo, Tatsuki; Kuriyama, Kazutaka; Tomonaga, Masao

doi:10.1111/j.1365-2141.1993.tb04709.x

Cited by 29 publications

(16 citation statements)

References 3 publications

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“…If one includes the five patients reported by the Rome group, the six patients presented here and previous case reports, 22 cases of MDS or AML (other than APL) occurring during the course of APL have been reported, [14][15][16][17][18][19][20][21][22][23][24][25] and their characteristics are shown in Table 2.…”

Section: Discussionmentioning

confidence: 99%

Myelodysplastic syndrome after acute promyelocytic leukemia: the European APL group experience

Lobe

Ferrant²,

Rigal‐Huguet

et al. 2003

Leukemia

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With improved treatment of acute promyelocytic leukemia (APL) by all trans retinoic acid (ATRA) combined to anthracycline-aracytin chemotherapy (CT), a larger number of those patients may be at risk of late complications. Recently, the Rome group reported five cases of myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML, non-APL) occurring during the course of 77 APL patients (6.5%) in complete remission (CR). From 1991 to 1998, we treated 677 newly diagnosed cases of APL, and 617 of them achieved CR with ATRA combined to CT (n ¼ 579) or CT alone (n ¼ 38); 246 of them received subsequent maintenance CT with 6 mercaptopurine and methotrexate. With a median follow-up of 51 months, 6 patients (0.97%) developed MDS, 13-74 months after the diagnosis of APL. In all six cases, t(15;17) and PMLRARalpha rearrangement were absent at the time of MDS diagnosis, and karyotype mainly showed complex cytogenetic abnormalities involving chromosomes 5 and/or 7, typical of MDS observed after treatment with alkylating agents, although none of the six patients had received such agents for the treatment of APL. Our findings suggest that MDS can indeed be a long-term complication in APL, although probably at lower incidence than that previously reported. Leukemia (2003) 17, 1600-1604. doi:10.1038/sj.leu.2403034 Keywords: acute promyelocytic leukemia-myelodysplastic syndrome; therapy related Introduction Acute promyelocytic leukemia (APL) is a specific type of acute myeloid leukemia (AML) characterized by the morphology of blast cells (M3 according to FAB classification), t(15;17) translocation that fuses the PML gene on chromosome 15 to the RAR alpha gene on chromosome 17, and by specific coagulopathy. 1,2 Anthracycline-aracytin (AraC) chemotherapy (CT), introduced in the 1960s, has yielded cure rates of 35-40% in APL, whereas combination of anthracycline-Ara C or anthracycline alone CT to all trans retinoic acid (ATRA), introduced in the early 1990s, has improved this cure rate to 65-70%, 3-6 thereby increasing the number of patients potentially at risk of late side effects of treatments. In the last 2 years, several case reports of myelodysplastic syndrome (MDS) or AML (different from APL), occurring during the course of APL, have been made. Recently, the Rome group 7 reported five cases of MDS in 77 (6.5%) APL patients treated with CT alone or ATRA combined to CT, suggesting that MDS/AML was possibly a major emerging problem in the follow-up of APL. Those findings prompted us to review cases of MDS or AML (non-APL) occurring during the evolution of APL patients included in multicenter trials of our European group. Patients and treatment PatientsBetween 1991 and 1998, we included 677 newly diagnosed cases of APL in APL 91 and APL 93 trials. Inclusion criteria were: diagnosis of APL based on morphological criteria and subsequently confirmed by presence of t(15;17) or PML-RAR alpha gene rearrangement, 8 age 75 years or less, and a minimum follow-up of 3 years.Treatment 9-11 APL 91 trial design: Patients were randomized to re...

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Section: Discussionmentioning

confidence: 99%

Myelodysplastic syndrome after acute promyelocytic leukemia: the European APL group experience

Lobe

Ferrant²,

Rigal‐Huguet

et al. 2003

Leukemia

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“…[13][14][15] Among chemotherapy agents, alkylating drugs and topoisomerase II inhibitors such as anthracyclines and epipodophillotoxins have been frequently associated with the development of tMDS-AML. Regarding tMDS-AML occurring after treatment for APL, sporadic cases have been reported to date, [16][17][18][19][20][21][22][23][24] but no studies have investigated this issue by analyzing large series of patients. We report here our experience with the development of tMDS-APL in a consecutive group of 77 patients with APL treated at a single institution.…”

Section: Introductionmentioning

confidence: 99%

Therapy-related myelodysplastic syndrome–acute myelogenous leukemia in patients treated for acute promyelocytic leukemia: an emerging problem

Latagliata¹,

Petti²,

Fenu³

et al. 2002

Blood

114

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The use of all-trans retinoic acid (ATRA) in combination with chemotherapy has markedly improved the prognosis for patients with acute promyelocytic leukemia (APL); the higher complete remission (CR) and survival rates now reported in this disease almost approach those obtained for other highly curable hematologic malignancies. Of 77 patients with APL who were consecutively treated at a single institution and who achieved CR after induction and consolidation therapy, 5 (6.5%) acquired therapy-related myelodysplasia (tMDS), acute myelogenous leukemia (AML), or both (tMDS-AML). Of these,

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“…3 Inhibition of DNA and RNA synthesis and the possibly related induction of apoptosis are the presumed mechanisms of action. Because T cell immunosuppression is a consequence, purine analogs could be successful in various autoimmune diseases, like rheumatoid arthritis, 4 even if autoimmune cytopenia, mostly hemolytic anemia, induced by fludarabine has been reported. 5 Our observation illustrates acquired hemophilia associated with CLL might be rapidly improved and cured with fludarabine and cyclophosphamide, without corticosteroids.…”

Section: The Editormentioning

confidence: 99%

“…Both the clonal and the temporal relationship between APL and the secondary AML subtype are usually obscure. [1][2][3][4] Recently, a chimeric M3:M2 case of acute promyelocytic leukemia was presented. 5 In November 1996, a 33-year-old Greek woman presented with anemia, thrombocytopenia and a white blood cell count of 28.0 × 10 9 /l with 60% blasts of typical M3 morphology.…”

Section: The Editormentioning

confidence: 99%

Simultaneous PML/RARα and AML 1/ETO gene rearrangements in a patient with acute myeloid leukemia

1999

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A unique case of t(15;17) acute promyelocytic leukaemia (M3) developing into acute myeloblastic leukaemia (M1) with t(7;21) at relapse

Cited by 29 publications

References 3 publications

Myelodysplastic syndrome after acute promyelocytic leukemia: the European APL group experience

Myelodysplastic syndrome after acute promyelocytic leukemia: the European APL group experience

Therapy-related myelodysplastic syndrome–acute myelogenous leukemia in patients treated for acute promyelocytic leukemia: an emerging problem

Simultaneous PML/RARα and AML 1/ETO gene rearrangements in a patient with acute myeloid leukemia

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