Inversion‐associated translocations in acute myelomonocytic leukemia with eosinophilia

Berger, Roland; Derré, Josette; Coniat, Maryvonne Le; Hebert, J; Romana, P. Serge; Jonveaux, Philippe

doi:10.1002/gcc.2870120110

Cited by 17 publications

(3 citation statements)

References 22 publications

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“…Inv(16)/t(16; 16), can be underestimated for technical reasons, such as poor chromosome morphology or analysis of cells belonging to a residual normal clone. Masked inv(16) due to inverted chromosomes being involved in translocations with other chromosomes or to submicroscopic rearrangements, has been detected in leukemias with normal karyotype or trisomy of chromosomes 8 and/or 22 (27, 28). Trisomy 8, 21, and 22 are additional karyotypic abnormalities in about half the patients with inv(16)/t(16; 16).…”

Section: Typical Chromosomal Changes Generating Fusion Transcriptsmentioning

confidence: 99%

GENETIC PROFILEOF ACUTE MYELOID LEUKEMIA

Mecucci

Rosati

Starza

2002

Rev Clin Exp Hematol

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Understanding genomic events and the cascade of their effects in cell function is crucial for identifying distinct subsets of acute myeloid leukemia and developing new therapeutic strategies. Conventional cytogenetics, fluorescence in situ hybridization investigations and molecular studies have provided much information over the past few years. This review will focus on major genomic mechanisms in acute myeloid luekemia and on the genes implicated in the pathogenesis of specific subtypes.

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Section: Typical Chromosomal Changes Generating Fusion Transcriptsmentioning

confidence: 99%

GENETIC PROFILEOF ACUTE MYELOID LEUKEMIA

Mecucci

Rosati

Starza

2002

Rev Clin Exp Hematol

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“…A number of cases of inv( 16) associated with chromosomal translocations have been described for the M4eo subtype of AML (reviewed in Berger et al, 1995). T h e phenomenon is poorly understood and may indeed be limited to inv(l6).…”

Section: B: T(l;))inv())(q212q263) With Der(l) and Der(3)mentioning

confidence: 99%

Cohabiting t(12;22) and inv(3) primary rearrangements in an acute myelomonocytic leukemia (FAB M4) cell line

MacLeod¹,

Hu²,

Kaufmann³

et al. 1996

Genes Chromosom. Cancer

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We describe the cytogenetic characterization of MUTZ-3, the first continuous cell line to be established from acute myelomonocytic leukemia (FAB M4) cells, exhibiting recurrent chromosomal rearrangements associated with this disease category. MUTZ-3 was established from peripheral blood taken at presentation from a 29-year-old male patient and carries the t(12;22)(p13.2;q11.2) associated with acute myelomonocytic leukemia (AMMoL), the inv(3)(q21.2q26.3) associated with multilineage acute myeloid leukemias (AML), and the inv(7)(p 14q35) associated with ataxia telangiectasia (A-T). There was no evidence that the patient was an A-T heterozygote. The breakpoint on chromosome 22 mapped between 5' BCR and D22S39, consistent with the G-banding assignment. Both inversions were translocation-associated and may be further examples of an association previously described in AML FAB M4eo with inv(16). We suggest that the combination of inv(3)/t(3;3) with t(12;22) may represent a new, nonrandom association in AML.

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“…In such cases, however, band 16q22 rather than 16p13 was mostly involved. Berger et al (1995), in performing FISH with the YAC 854E2, showed that what appeared as variant translocations of 16q22 in two cases of AML-M4Eo contained a masked inv(16). In both cases, an inversion involving MYH11 and CBFB plus a translocation occurred in the same chromosome 16 as two independent events, with different breakpoints.…”

Section: Discussionmentioning

confidence: 99%

Rearrangement between the MYH11 gene at 16p13 and D12S158 at 12p13 in a case of acute myeloid leukemia M1 (AML‐M1)

Starza

Włodarska

Matteucci

et al. 1998

Genes Chromosom. Cancer

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A case of acute myeloid leukemia (AML) M1 with bone marrow eosinophilia was characterized by cytogenetics and fluorescence in situ hybridization (FISH). A complex karyotype including a der(12)t(12;17)(p12-13;q11) and a der(16)t(16;20)(p13;p11) was found at diagnosis. FISH studies with probes for chromosome 16 and for the short arm of chromosome 12 showed even more complex rearrangements. Analysis with a panel of probes for 12p showed that D12S158 spanned the breakpoint on the der(12). Unexpectedly, FISH signals were found on the der(12) and on the der(6) at band p13, the site of juxtaposition between the short arm of chromosome 16 and chromosome 20. Moreover, both YAC 854E2, containing the MYH11 gene, and cosmid ZIT133, encompassing the MYH11 breakpoint in inv(16) and t(16;16) of AML-M4 with eosinophilia, demonstrated fluorescent signals on the normal 16, on the der(16), and on the der(12). These data clearly support a reciprocal exchange between D12S158 at 12p13.3 and the MYH11 gene at 16p13. In addition, experiments with two PAC clones for the CBFB gene at 16q22 excluded the presence of a masked inv(16). An interstitial deletion, independent from the translocation and flanked by VWF and KRAS2, was also detected on the der(12).

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Inversion‐associated translocations in acute myelomonocytic leukemia with eosinophilia

Cited by 17 publications

References 22 publications

GENETIC PROFILEOF ACUTE MYELOID LEUKEMIA

GENETIC PROFILEOF ACUTE MYELOID LEUKEMIA

Cohabiting t(12;22) and inv(3) primary rearrangements in an acute myelomonocytic leukemia (FAB M4) cell line

Rearrangement between the MYH11 gene at 16p13 and D12S158 at 12p13 in a case of acute myeloid leukemia M1 (AML‐M1)

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