Cytogenetic studies on 519 consecutive de novo acute nonlymphocytic leukemias

Berger, Roland; Flandrin, Georges; Bernheim, Alain; Coniat, Maryvonne Le; Vecchione, Danièle; Pacot, Annie; Derré, Josette; Daniel, Marie‐Thérèse; Valensi, Françoise; Sigaux, François; Ochoa-Noguera, Maria Elena

doi:10.1016/0165-4608(87)90026-4

Cited by 148 publications

(51 citation statements)

References 18 publications

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“…The balanced translocation has previously been reported to be preferentially associated with AML M4. Seven reported cases showed this translocation either as the sole abnormality or as part of a simple karyotype in six cases of AML M4 [20][21][22][23][24] and one case of AML M5. 25 The MLL partner gene at 1q21 (AF1q) has been characterised.…”

Section: A Overall Cases In 'Other' Groupmentioning

confidence: 99%

Ten novel 11q23 chromosomal partner sites

Cuneo²,

et al. 1998

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The MLL gene located at 11q23 has been described as a 'promiscuous' gene due its involvement with a large number of genetic partners. The EU Concerted Action Workshop on 11q23 provided 550 cases for study of which 82 showed abnormalities which did not involve the established translocations or deletion of 11q23. In these 'other' cases, which included inversions and duplications, 11q23 was found to be involved with 25 chromosome partners of which 10 had not been previously reported. These were 1q31, 4p11, 6q13, 8q21, 10q22, 10q25, 11q11, 11q21, 13q34 and 18q23. This study demonstrated the value of the Workshop, in confirming the diversity of chromosomal partner sites involved with 11q23 and in the identification of new partners.

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Section: A Overall Cases In 'Other' Groupmentioning

confidence: 99%

Ten novel 11q23 chromosomal partner sites

Cuneo²,

et al. 1998

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“…For instance, several reports (Berger et al, 1987;Marosi et al, 1992;Harrison et al, 1998;Satake et al, 1999) have shown the existence of a molecular rearrangement of the MLL gene with a not yet identified fusion partner gene in 17q23, where the SEPT4 gene is located (Table 2). Furthermore, the existence of known MLL partner genes in chromosomal bands where septin genes are mapped (Table 2) does not exclude the possibility that they also may be rearranged with MLL.…”

Section: Mll-sept2 Fusion Gene In Aml N Cerveira Et Almentioning

confidence: 99%

SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23)

et al. 2006

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We have identified a new mixed lineage leukemia (MLL) gene fusion partner in a patient with treatment-related acute myeloid leukemia (AML) presenting a t(2;11)(q37;q23) as the only cytogenetic abnormality. Fluorescence in situ hybridization demonstrated a rearrangement of the MLL gene and molecular genetic analyses identified a septin family gene, SEPT2, located on chromosome 2q37, as the fusion partner of MLL. RNA and DNA analyses showed the existence of an in-frame fusion of MLL exon 7 with SEPT2 exon 3, with the genomic breakpoints located in intron 7 and 2 of MLL and SEPT2, respectively. Search for DNA sequence motifs revealed the existence of two sequences with 94.4% homology with the topoisomerase II consensus cleavage site in MLL intron 7 and SEPT2 intron 2. SEPT2 is the fifth septin family gene fused with MLL, making this gene family the most frequently involved in MLL-related AML (about 10% of all known fusion partners). The protein encoded by SEPT2 is highly homologous to septins 1, 4 and 5 and is involved in the coordination of several key steps of mitosis. Further studies are warranted to understand why the septin protein family is particularly involved in the pathogenesis of MLL-associated leukemia.

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“…They reported that a favourable karyotype was more frequent in patients whose first remissions were at least 12 months, while the opposite was found in patients with an unfavourable karyotype. In 1989, Keating et al 22 reported that the karyotype was only predictive for patients with inv (16) or t1 (5,17) with a relapse within 12 months after first CR. We have previously reported that the proportion of patients with a favourable karyotype is high among patients with a duration of second CR of more than 2 years.…”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3][4] Several pretreatment factors such as age, performance status, leucocyte count and karyotype predict the outcome, but karyotype is certainly the most important prognostic factor for the rate of complete remission (CR), overall survival (OS) and disease-free survival (DFS). [5][6][7][8][9][10][11][12] Four large studies (and several smaller ones) demonstrated that the estimated OS at 5 years is around 35-65% among patients with favourable cytogenetics, while it is between 15 and 40% among patients with intermediate and below 20% among patients with adverse cytogenetics. [13][14][15][16] The prognosis of patients after a first relapse of AML is generally poor.…”

Section: Introductionmentioning

confidence: 99%

Impact of cytogenetics on the prognosis of adults with de novo AML in first relapse

Weltermann

Fonatsch²,

Haas

et al. 2003

Leukemia

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Karyotype is an important prognostic factor in patients with newly diagnosed acute myeloblastic leukaemia (AML). The prognostic value of cytogenetics on the outcome of patients with AML in relapse has not yet been well defined. We analysed the clinical outcome of 152 patients with de novo, chemotherapy-treated AML in first relapse according to the cytogenetic classification of the United Kingdom Medical Research Council. The rate of second complete remission (CR) (88, 64 and 36%) and the probability of survival at 3 years (43, 18 and 0%) were significantly different between the favourable, intermediate and adverse cytogenetic risk groups, respectively. Compared to the favourable group, the relative risk (RR) of death (multivariate analyses) was 2.6 (confidence interval (CI): 1.5-4.4, Po0.001) for the intermediate and 3.7 (CI: 1.7-7.9, P ¼ 0.001) for the adverse group. The prognostic value of the duration of first CR was confirmed (RR of death: 2.0 (CI: 1.0-4.0) for each additional year in first CR), whereas the FLT3 mutation obtained at diagnosis did not markedly influence the outcome of patients with AML in relapse. In conclusion, our results indicate that both karyotype and the duration of first CR are independent prognostic factors for patients with de novo AML in first relapse.

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Cytogenetic studies on 519 consecutive de novo acute nonlymphocytic leukemias

Cited by 148 publications

References 18 publications

Ten novel 11q23 chromosomal partner sites

Ten novel 11q23 chromosomal partner sites

SEPT2 is a new fusion partner of MLL in acute myeloid leukemia with t(2;11)(q37;q23)

Impact of cytogenetics on the prognosis of adults with de novo AML in first relapse

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