Association of t(15;17) and t(8;21) in the initial phase of an acute promyelocytic leukemia

Charrin, C; Ritouet, Danièle; Campos, Lydia; Devaux, Yves; Archimbaud, E; Fraisse, J; Fière, D; Germain, D

doi:10.1016/0165-4608(92)90108-k

Cited by 17 publications

(13 citation statements)

References 14 publications

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“…Additional chromosome rearrangements including t(8;21) and t(15;17) are rarely seen in APL patients treated initially with ATRA plus chemotherapy [11,13,14,15]. Two case studies reported a coexistence of t(8;21) and t(15;17) chromosomal anomalies in their patients at the time of diagnosis, and they concluded that t(8;21) may have been the first event to originate from an early leukemic clone, while t(15;17) was acquired later in the course of the disease [11,13]. Charrin et al detected 2 clones at the initial phase of an AML including 46,XX,t(15;17) and 46,XX,t(8;21),t(15;17).…”

Section: Discussionmentioning

confidence: 99%

“…Charrin et al detected 2 clones at the initial phase of an AML including 46,XX,t(15;17) and 46,XX,t(8;21),t(15;17). Relapse occurred after 12 months of complete remission with typical APL syndrome when t(15;17) alone was the most predominant [11]. Movafagh et al [16] reported a female patient in whom 2 French-American-British (FAB)-specific chromosome aberrations evolved from a single leukemic clone and co-expressed t(15;17) and t(8;21).…”

Section: Discussionmentioning

confidence: 99%

“…Chromosomal abnormalities accompanying t(15;17) are reported in 23%-39% of APL cases [2,6,7,8,9,10]. Additional chromosome rearrangements including t(8;21) and t(15;17) are rarely seen in APL patients [11,12]. However, the clinical impact of these secondary anomalies has not been clearly elucidated yet.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Co-expression of t(15;17) and t(8;21) in a Case of Acute Promyelocytic Leukemia: Review of the Literature

Uz¹,

Eliaçık²,

Işık³

et al. 2013

tjh

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Additional chromosomal abnormalities in acute myelogenous leukemia have been identified as one of the most important prognostic factors. Favorable chromosomal changes such as t(8;21), inv(16), and t(15;17) are associated with higher rates of complete remission and event-free survival. Translocation (15;17) characterizes acute promyelocytic leukemia (APL) (French-American-British class M3) in almost all patients. Secondary chromosomal abnormalities are also present in approximately 23%-29% of patients with newly diagnosed APL. The prognostic implications of t(8;21) and other secondary cytogenetic aberrations in APL are reviewed here. We present a 47-year-old woman diagnosed with APL whose initial cytogenetic analysis included both t(8;21) and t(15;17). The initial induction chemotherapy included 3 days of idarubicin (12 mg/m2/day) and daily all-trans retinoic acid (ATRA; 45 mg/m2/day). At the sixth week of treatment, a control bone marrow biopsy was found to be normocellular, t(15;17) bcr3 and t(8;21) were negative, and t(15;17) bcr1 fusion transcripts were reduced from 5007 (1.78525699%) copies per 1 µg RNA to 40 (0.00062020%) with real-time quantitative polymerase chain reaction. Consolidation with 4 days of idarubicin (5 mg/m2/day), ATRA (45 mg/m2/day for 15 days), and cytarabine (1 g/m2/day for 4 days) was then started. However, the patient became pancytopenic and had neutropenic fever after consolidation treatment. Unfortunately, she died 3 months after the time of APL diagnosis, due to acute respiratory distress syndrome-like respiratory problems and multiorgan dysfunction requiring respiratory support and hemodialysis. Conflict of interest:None declared.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Co-expression of t(15;17) and t(8;21) in a Case of Acute Promyelocytic Leukemia: Review of the Literature

Uz¹,

Eliaçık²,

Işık³

et al. 2013

tjh

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“…9,20 Cytogenetic or molecular confirmation of genetic APL in cases with primary clinical ATRA resistance is important, because several instances of leukemic chimeras have been reported in which APL cells are admixed with alternative leukemia cells, most frequently t(8;21)/AML1-ETO-positive cells. [26][27][28][29][30] For example, in the INT0129 trial, a case that was PML-RAR␣-positive but lacked the t(15;17) in the few analyzable metaphase cells (as occurs in ෂ15% of cases analyzed) was crossed over to the chemotherapy induction arm of the protocol because of ATRA toxicity (but also with a poor initial response) and, after initially achieving CR, the patient relapsed with PML-RAR␣-negative AML. 31 Similar instances have been cited in other studies involving ATRA induction as a single agent 32 or in combination with chemotherapy.…”

Section: Spotlightmentioning

confidence: 99%

Retinoic acid resistance in acute promyelocytic leukemia

2002

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Primary resistance of PML-RAR␣-positive acute promyelocytic leukemia (APL) to the induction of clinical remission (CR) by all-trans retinoic acid (ATRA) is rare but markedly increases in frequency after Ն2 relapses from chemotherapy-induced CRs. Nevertheless, even in de novo cases, the primary response of ATRA-naive cases is variable by several measures, suggesting involvement of heterogeneous molecular elements. Secondary, acquired ATRA resistance occurs in most patients treated with ATRA alone and in many patients who relapse from combination ATRA chemotherapy regimens despite limited ATRA exposure. Although early studies suggested that an adaptive hypercatabolic response to pharmacological ATRA levels is the principal mechanism of ATRA resistance, recent studies suggest that molecular disturbances in APL cells have a predominant role, particularly if disease relapse occurs a few months after discontinuing ATRA therapy. This review summarizes the systemic and APL cellular elements that have been linked to clinical ATRA resistance with emphasis on identifying areas of deficient information and important topics for further investigation. Overall, the subject review strongly supports the hypothesis that, although APL is an infrequent and nearly cured disease, much can be gained by understanding the complex relationship of ATRA resistance to the progression and relapse of APL, which has important implications for other leukemias and malignancies.

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“…t (15;17) concomitant with other specific translocations is rare, reflecting disease evolution and progression. [12][13][14] In rare cases, variant chromosome translocations have been reported, which fuse RAR␣ gene with partner genes other than PML, such as t(11;17)(q23;q21), 15 t(5;17)(q35;q21), 16 t(11;17)(q13;q21) 17 and dup(17)(q21.3q23). 18 Apart from the cytogenetic heterogeneity, molecular studies on APL patients also revealed heterogeneity of the PML-RAR␣ transcripts as a result of the variability of the chromosome 15 breakpoints.…”

Section: Introductionmentioning

confidence: 99%

Molecular cytogenetic characterization and clinical relevance of additional, complex and/or variant chromosome abnormalities in acute promyelocytic leukemia

Zhao

Xiong

et al. 2001

Leukemia

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Acute promyelocytic leukemia (APL) is characterized by typical morphological manifestation, t(15;17) translocation and active response to all-trans retinoic acid (ATRA) in the great majority of patients. However, a subset of APL cases may present atypical phenotypic, cytogenetic or molecular features at different stages of the disease. The biological and clinical significance of these features sometimes remains obscure. In this study, 284 APL patients were cytogenetically analyzed and precise diagnosis was performed according to the molecular cytogenetic results. Twenty-six APL patients were identified as having additional, complex and/or variant chromosomal abnormalities at diagnosis or at relapse, 16 of them being further analyzed using fluorescence in situ hybridization (FISH) or chromosome painting (CP). Interestingly, some of these chromosomal aberrations were found to be associated with atypical morphology and/or drug response, indicating a genotype-phenotype correlation. Analysis of the complex karyotype may also allow a better understanding of the levels of cellular origin of the leukemogenesis. Examination of the remission induction and survival data showed that the presence of the additional/complex chromosome abnormalities was related to the prognosis in both primarily diagnosed and relapsed patients in this series. Leukemia (2001) 15, 1359-1368.

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Association of t(15;17) and t(8;21) in the initial phase of an acute promyelocytic leukemia

Cited by 17 publications

References 14 publications

Co-expression of t(15;17) and t(8;21) in a Case of Acute Promyelocytic Leukemia: Review of the Literature

Co-expression of t(15;17) and t(8;21) in a Case of Acute Promyelocytic Leukemia: Review of the Literature

Retinoic acid resistance in acute promyelocytic leukemia

Molecular cytogenetic characterization and clinical relevance of additional, complex and/or variant chromosome abnormalities in acute promyelocytic leukemia

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