Myelodysplastic Syndrome Preceding Acute Myelomonocytic Leukemia with Dysplastic Marrow Eosinophilia and Inv(16)

Horiike, Shigeo; Misawa, Shinichi; Nishida, Kazuhiro; Nishigaki, H; Tsuda, S; Takino, Tatsuro; Abe, Tatsuo

doi:10.1159/000205368

Cited by 15 publications

(10 citation statements)

References 10 publications

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“…Therefore, the diagnosis of MDS-Eo requires careful exclusion of other hematological disorders. To our knowledge, clonal eosinophilia with MDS has been previously reported in 5 cases [2, 3, 4, 5, 6]. In the case presented here, chromosomal aberration was identified in eosinophilic metaphase spreads by means of simple Giemsa staining, thus indicating that eosinophilia in our case was clonal proliferation.…”

Section: Introductionsupporting

confidence: 52%

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Myelodysplastic Syndrome with Clonal Eosinophilia Accompanied by Eosinophilic Pulmonary Interstitial Infiltration

et al. 2000

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We report a case of de novo myelodysplastic syndrome with clonal eosinophilia (MDS-Eo) and eosinophilic pulmonary interstitial infiltration, confirmed by autopsy. Cytogenetic study using Giemsa banding identified 47,XY,+1,der(1;7)(q10;p10),+8 in the marrow cells. Simple Giemsa staining revealed the same chromosomal aberration in metaphase spreads with eosinophilic granules, indicating the clonal proliferation of eosinophils. To our knowledge, our case is the 6th reported case of MDS-Eo with cytogenetically confirmed clonal eosinophilia, and the first autopsy of MDS-Eo. A review of the literature combined with our findings suggests that this type of chromosomal aberration might be involved in the as yet unknown pathogenesis of MDS-Eo.

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Section: Introductionsupporting

confidence: 52%

“…To ascertain the clonality of the eosinophils, metaphase spreads overlaid with eosinophilic granules were analyzed as described previously (fig. 3b) [1, 2]. Briefly, by omitting trypsin treatment, we could observe eosinophilic cytoplasmic granules in some of the metaphase spreads, which were recognized as eosinophils.…”

Section: Case Reportmentioning

confidence: 99%

Myelodysplastic Syndrome with Clonal Eosinophilia Accompanied by Eosinophilic Pulmonary Interstitial Infiltration

et al. 2000

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“…These abnormalities included t(5;12)(q33;p13), 20 inv16(p13q22), [17][18][19] and other abnormalities in chromosomes 7 or 16. 9,23,32,33 The t(5;12)(q33;p13) abnormality is less common but appears to be relevant for the pathogenesis of the eosinophilia.…”

Section: Discussionmentioning

confidence: 99%

“…In previous reports, bone marrow eosinophilia or basophilia in MDS was observed in patients having complex karyotypes, 9,11 a chromosome 7 abnormality, 12 i(17q), 13 t(6;9), [14][15][16] inv16, [17][18][19] or t(5;12). 20 In our study, t(6;9) was observed in only 2 patients and neither inv16 nor t(5;12) was detected.…”

Section: Cytogeneticsmentioning

confidence: 99%

Prevalence and clinical characteristics of myelodysplastic syndrome with bone marrow eosinophilia or basophilia

Maekawa

Handa

Yokohama

et al. 2003

Blood

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By retrospectively analyzing 288 patients with de novo myelodysplastic syndrome (MDS), we sought to determine the prevalence and clinical characteristics of bone marrow eosinophilia and basophilia that were detected at presentation. Bone marrow eosinophilia and basophilia were defined as a differential count of each cell type exceeding 5.0% and 1.0%, respectively. Of 288 patients with MDS, 36 (12.5%) fulfilled this criterion for bone marrow eosinophilia (MDS-Eos); 34 patients (11.8%) showed basophilia (MDS-Bas), and 11 (3.8%) satisfied both criteria (MDSEosBas). The remaining 229 patients had neither eosinophilia nor basophilia in their bone marrow (MDS ؊/؊ ) at presentation. Cytogenetic analysis was carried out on unstimulated bone marrow cells obtained from 264 patients. When the cytogenetic categorization of the IPSS (International Prognostic Scoring System) for MDS was applied, significantly higher numbers of MDS-Eos and MDS-Bas patients had chromosomal abnormalities carrying intermediate or poor prognosis, compared with the MDS ؊/؊ patients. Specific chromosomal abnormalities and complex karyotypes were associated with MDS-Eos and/or MDS-Bas. In accordance with these results, the overall survival rate was significantly lower, and the evolution to acute myelogenous leukemia (AML) occurred more frequently in the MDS-Eos and MDSBas than in the MDS ؊/؊ patients. Multivariate analysis demonstrated that bone marrow basophilia was an independent risk factor for evolution to AML. Our study indicates that bone marrow eosinophilia and basophilia in patients with MDS predict a poorer prognosis. (Blood. 2003;

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“…Alterations of the PEBP2␣B and PEBP2␤ genes have been associated with myelodysplasia (8,(40)(41)(42)(43). Neutrophils generated in vitro from PEBP2␤MYH11 transgenic bone marrow displayed unusual morphology.…”

Section: Discussionmentioning

confidence: 99%

The PEBP2 β MYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasia

Lagasse

Atwater

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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Chromosomal translocations involving the genes encoding the alpha and beta subunits of the Pebp2͞Cbf transcription factor have been associated with human acute myeloid leukemia and the preleukemic condition, myelodysplasia. Inv(16)(p13;q22) fuses the gene encoding the beta subunit of Pebp2 to the MYH11 gene encoding a smooth muscle myosin heavy chain (Smmhc). To examine the effect of the inv(16)(p13;q22) on myelopoiesis, we used the hMRP8 promoter element to generate transgenic mice expressing the Pebp2␤Smmhc chimeric fusion protein in myeloid cells. Neutrophil maturation was impaired in PEBP2␤MYH11 transgenic mice. Although the transgenic mice had normal numbers of circulating neutrophils, their bone marrow contained increased numbers of immature neutrophilic cells, which exhibited abnormal characteristics. In addition, PEBP2␤MYH11 inhibited neutrophilic differentiation in colonies derived from hematopoietic progenitors. Coexpression of both PEBP2␤MYH11 and activated NRAS induced a more severe phenotype characterized by abnormal nuclear morphology indicative of granulocytic dysplasia. These results show that PEBP2␤MYH11 can impair neutrophil development and provide evidence that alterations of Pebp2 can contribute to the genesis of myelodysplasia.

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Myelodysplastic Syndrome Preceding Acute Myelomonocytic Leukemia with Dysplastic Marrow Eosinophilia and Inv(16)

Cited by 15 publications

References 10 publications

Myelodysplastic Syndrome with Clonal Eosinophilia Accompanied by Eosinophilic Pulmonary Interstitial Infiltration

Myelodysplastic Syndrome with Clonal Eosinophilia Accompanied by Eosinophilic Pulmonary Interstitial Infiltration

Prevalence and clinical characteristics of myelodysplastic syndrome with bone marrow eosinophilia or basophilia

The PEBP2 β MYH11 fusion created by Inv(16)(p13;q22) in myeloid leukemia impairs neutrophil maturation and contributes to granulocytic dysplasia

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