5q– myelodysplastic syndromes: chromosome 5q genes direct a tumor-suppression network sensing actin dynamics

Eisenmann, Kathryn M.; Dykema, Karl; Matheson, Stephen; Kent, Nicola; DeWard, Aaron D.; West, Richard; Tibes, Raoul; Furge, Kyle A.; Alberts, Arthur S.

doi:10.1038/onc.2009.207

Cited by 76 publications

(59 citation statements)

References 111 publications

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“…12 Our AML-CDR (from 5q32 to 5q33.2) contains 101 genes expressed in bone marrow (http://www.ncbi.nlm.nih.gov/projects/ mapview/) and differs from CDR2 described by Eisenmann et al 12 This commonly deleted segment is closer to the CDR1, present in 5q-syndrome patients (Figure 2). In contrast with previously published data, 4,7,12,13 AML-CDR is distal to band 5q31. These observations highlight the heterogeneity of 5q deletions in myeloid neoplasms.…”

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confidence: 89%

“…In a review based on the studies that had defined the common deleted region of chromosome 5, 5 --10 Eisenmann et al 12 reported two CDRs: CDR1 (from bands 5q32 to 5q33.1) in 5q-syndrome and CDR2 (from 5q31.1 to 5q31.2) in aggressive MDS and AML patients (Figure 2). Comparison with the literature data is difficult because of differences in disease classification (5q-syndrome versus 5q deletion, aggressive disease and so on), lack of precision of the karyotypes, lack of verification by FISH or array CGH and so on, which could explain discrepancies between our results and those previously reported.…”

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confidence: 99%

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Molecular characterization of deletions of the long arm of chromosome 5 (del(5q)) in 94 MDS/AML patients

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Molecular characterization of deletions of the long arm of chromosome 5 (del(5q)) in 94 MDS/AML patients

et al. 2012

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“…It is associated with refractory anemia, thrombocytosis, hypolobulated megakaryocytes and low risk of evolving into AML. 16 Because deletion of 5q represents the major cytogenetic abnormality associated with MDS, it has been hypothesized that this region may contain an important MDS suppressor gene. 16,18 One such candidate is the NPM (Nucleophosmin) gene, located in the 5q region.…”

Section: Mds Mouse Models Of Chromosomal Deletions: Candidate Genes Fmentioning

confidence: 99%

“…16 Because deletion of 5q represents the major cytogenetic abnormality associated with MDS, it has been hypothesized that this region may contain an important MDS suppressor gene. 16,18 One such candidate is the NPM (Nucleophosmin) gene, located in the 5q region. Mutations of the NPM1 gene have also been found in 4.4% of MDS patients.…”

Section: Mds Mouse Models Of Chromosomal Deletions: Candidate Genes Fmentioning

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Engineering mouse models with myelodysplastic syndrome human candidate genes; how relevant are they?

2012

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Myelodysplastic syndromes represent particularly challenging hematologic malignancies that arise from a large spectrum of genetic events resulting in a disease characterized by a range of different presentations and outcomes. Despite efforts to classify and identify the key genetic events, little improvement has been made in therapies that will increase patient survival. Animal models represent powerful tools to model and study human diseases and are useful pre-clinical platforms. In addition to enforced expression of candidate oncogenes, gene inactivation has allowed the consequences of the genetic effects of human myelodysplastic syndrome to be studied in mice. This review aims to examine the animal models expressing myelodysplastic syndrome-associated genes that are currently available and to highlight the most appropriate model to phenocopy myelodysplastic syndrome disease and its risk of transformation to acute myelogenous leukemia. ©2013 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2012.069385 ABSTRACTMouse models myelodysplastic syndrome human candidate genes haematologica | 2013; 98 (1) 11 Figure 1. Mouse models to study malignant hematologic disease. Several strategies can be employed to create mouse models of disease. Candidate genes can be introduced into the germline under the control of appropriate promoters to drive expression in certain cell compartments. Knock-out strategies create gene deficient mice, whilst knock-in strategies use the endogenous promoters; but again these tend to be conditional systems requiring specific promoters to determine in which cell the genes are introduced. Transduction of bone marrow and reinfusion is a powerful tool. Xenograft models are theoretically the best if the techniques involved can be improved.

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Myelodysplastic Syndromes

2007

Veterinary Comparative Hematopathology

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SynopsisThe myelodysplastic syndromes are a diverse group of clonal stem cell disorders characterized by ineffective hematopoiesis, peripheral cytopenias, and an increased propensity to evolve to acute myeloid leukemia. The molecular pathogenesis of these disorders is poorly understood, but recurring chromosomal abnormalities occur in ~50% of cases, and are the focus of much investigation. The availability of newer molecular techniques has allowed the identification of additional genetic aberrations, including mutations and epigenetic changes of prognostic and potential therapeutic importance. This review will focus on the key role of cytogenetic analysis in MDS in the context of the diagnosis, prognosis, and pathogenesis of these disorders.Keywords myelodysplastic syndromes; cytogenetics; molecular genetics; diagnosis; prognosis; classification IntroductionThe myelodysplastic syndromes (MDS) include a large spectrum of clonal hematopoietic stem cell disorders that are characterized by peripheral cytopenia(s), morphologic dysplasia, ineffective hematopoiesis, and a variable propensity to transform to acute myeloid leukemia (AML). 1,2 The cytopenia can be limited to a single cell line resulting in anemia, This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript thrombocytopenia, or neutropenia, and can be chronic and somewhat indolent, or profound involving all three lineages with life-threatening consequences. The morphologic dysplasia associated with the ineffective hematopoiesis may be subtle and difficult to recognize but, in some cases, it can be impressive and evident in both the bone marrow and peripheral blood. The variable increase in blasts relates, in part, to the risk for transformation to AML, although progression is not solely dependent on the blast percentage. MDS is a disease of older adults with a median age at diagnosis of ~70 years 3 . Other risk factors for the development of MDS include tobacco use and exposure to solvents, such as benzene and agricultural chemicals. In ~10-15% of cases, the disease arises as a late complication of cytotoxic therapy (radiotherapy and/or chemotherapy) for a prior disorder, and is referred to as a therapy-related myeloid neoplasm (t-MN). MDS is frequently associated with clonal cytogenetic abnormalities, of significant prognostic 4,5 and emerging therapeutic importance. An in-depth analysis of some of these is providing significant insights into underlying molecular alterations, which may hold clues to unraveling the pathogenesis of these disorders. This review will focus on the ...

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5q– myelodysplastic syndromes: chromosome 5q genes direct a tumor-suppression network sensing actin dynamics

Cited by 76 publications

References 111 publications

Molecular characterization of deletions of the long arm of chromosome 5 (del(5q)) in 94 MDS/AML patients

Molecular characterization of deletions of the long arm of chromosome 5 (del(5q)) in 94 MDS/AML patients

Engineering mouse models with myelodysplastic syndrome human candidate genes; how relevant are they?

Myelodysplastic Syndromes

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