Leukemic Cluster Growth in Culture Is an Independent Risk Factor for Acute Myeloid Leukemia and Short Survival in Patients with Myelodysplastic Syndrome

Bernimoulin, Michael; Stangel, Martin; Thewis, André; Jotterand, Martine; Gratwohl, Aloïs; Nissen, C

doi:10.1159/000140675

Cited by 5 publications

(2 citation statements)

References 59 publications

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“…This patient's cells had abnormal growth patterns, as demonstrated by the low number of colonies per plate, low cell counts per colony as well as a delayed colony growth. Our observations concerning MDS colony formation agree with those reported by others (Polychronopoulou et al, 2004;Bernimoulin et al, 2008). Nevertheless, we were able to isolate six distinct myeloid clusters.…”

Section: Discussionsupporting

confidence: 92%

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Clonal heterogeneity in childhood myelodysplastic syndromes—Challenge for the detection of chromosomal imbalances by array‐CGH

Praulich

Tauscher

Göhring

et al. 2010

Genes Chromosomes & Cancer

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To evaluate whether copy number alterations (CNAs) are present that may contribute to disease development and/or progression of childhood myelodysplastic syndromes (MDS), 36 pediatric MDS patients were analyzed using array-based comparative genome hybridization (aCGH). In addition to monosomy 7, the most frequent chromosome aberration in childhood MDS, novel recurrent CNAs were detected. They included a loss of 3p14.3-p12.3, which contains the putative tumor suppressor gene FHIT, a loss of 7p21.3-p15.3, a loss of 9q33.3-q34.3 (D184) and microdeletions in 17p11.2, 6q23 containing MYB, and 17p13 containing TP53. In this small patient cohort, patients without CNA, patients with monosomy 7 only and patients with one CNA in addition to monosomy 7 did not differ in their survival. As expected, all patients with complex karyotypes, including two patients with deletions of TP53, died. A challenge inherent to aCGH analysis of MDS is the low percentage of tumor cells. We evaluated several approaches to overcome this limitation. Genomic profiles from isolated granulocytes were of higher quality than those from bone marrow mononuclear cells. Decreased breakpoint calling stringency increased recognition of CNAs present in small clonal populations. However, further analysis using a custom-designed array showed that these CNAs often did not confirm the findings from 244k arrays. In contrast, constitutional CNVs were reliably detected on both arrays. Moreover, aCGH on amplified DNA from distinct myeloid clusters is a new approach to determine CNAs in small subpopulations. Our results clearly emphasize the need to verify array-CGH results by independent methods like FISH or quantitative PCR.

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Section: Discussionsupporting

confidence: 92%

“…As previously reported (Polychronopoulou et al, 2004;Bernimoulin et al, 2008), colony formation for Figure 3. Comparison of monosomy 7 detection rate by qPCR, FISH, karyotyping and aCGH.…”

Section: Genomic Profiles Of Single Myeloid Clusterssupporting

confidence: 79%

Clonal heterogeneity in childhood myelodysplastic syndromes—Challenge for the detection of chromosomal imbalances by array‐CGH

Praulich

Tauscher

Göhring

et al. 2010

Genes Chromosomes & Cancer

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Are myelodysplastic syndromes and acute myeloid leukemia one disease?

Gale¹,

Bennett²

2009

Leukemia Research

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Iron overload impairs proliferation of erythroid progenitors cells (BFU-E) from patients with myelodysplastic syndromes

et al. 2013

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In patients with myelodysplastic syndromes (MDS) iron overload caused by long-term red blood cell transfusions is an important factor for comorbidity especially in low-risk MDS. In this report we present the results of a comparative study based on colony formation assays of hematopoietic cells in MDS patients with and without iron overload. We demonstrate that iron overload suppresses the proliferation of erythroid progenitors cells (BFU-E), while the myeloid compartment (CFU-GM) was not found to be affected. Even patients with slightly elevated ferritin values show an impaired proliferation capacity in comparison to patients with normal ferritin levels. Furthermore, we show that this negative impact is reversible by sufficient iron chelation therapy.

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Leukemic Cluster Growth in Culture Is an Independent Risk Factor for Acute Myeloid Leukemia and Short Survival in Patients with Myelodysplastic Syndrome

Abstract: a significant predictive value in addition to established prognostic factors in MDS. Leukemic growth identifies a subpopulation of MDS patients with poor prognosis.

Cited by 5 publications

References 59 publications

Clonal heterogeneity in childhood myelodysplastic syndromes—Challenge for the detection of chromosomal imbalances by array‐CGH

Clonal heterogeneity in childhood myelodysplastic syndromes—Challenge for the detection of chromosomal imbalances by array‐CGH

Are myelodysplastic syndromes and acute myeloid leukemia one disease?

Iron overload impairs proliferation of erythroid progenitors cells (BFU-E) from patients with myelodysplastic syndromes

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