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Relevant bibliographies by topics / Myelodysplastic

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Academic literature on the topic 'Myelodysplastic'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Myelodysplastic"

1

Giagounidis, A. A. N. "Myelodysplasia or myelodysplastic syndrome?" Leukemia Research 33, no. 8 (August 2009): 1019. http://dx.doi.org/10.1016/j.leukres.2009.02.012.

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Kawase, Yuuki, Masashi Ohe, Haruki Shida, Tetsuya Horita, Ken Furuya, and Satoshi Hashino. "Methotrexate-induced myelodysplasia mimicking myelodysplastic syndrome." Blood Research 53, no. 4 (2018): 268. http://dx.doi.org/10.5045/br.2018.53.4.268.

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Ohe, Masashi. "Azathioprine-induced Myelodysplasia Mimicking Myelodysplastic Syndrome." Ewha Medical Journal 42, no. 3 (2019): 46. http://dx.doi.org/10.12771/emj.2019.42.3.46.

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Natelson, Ethan A., and David Pyatt. "Acquired Myelodysplasia or Myelodysplastic Syndrome: Clearing the Fog." Advances in Hematology 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/309637.

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Myelodysplastic syndromes (MDS) are clonal myeloid disorders characterized by progressive peripheral blood cytopenias associated with ineffective myelopoiesis. They are typically considered neoplasms because of frequent genetic aberrations and patient-limited survival with progression to acute myeloid leukemia (AML) or death related to the consequences of bone marrow failure including infection, hemorrhage, and iron overload. A progression to AML has always been recognized among the myeloproliferative disorders (MPD) but occurs only rarely among those with essential thrombocythemia (ET). Yet, the World Health Organization (WHO) has chosen to apply the designation myeloproliferative neoplasms (MPN), for all MPD but has not similarly recommended that all MDS become the myelodysplastic neoplasms (MDN). This apparent dichotomy may reflect the extremely diverse nature of MDS. Moreover, the term MDS is occasionally inappropriately applied to hematologic disorders associated with acquired morphologic myelodysplastic features which may rather represent potentially reversible hematological responses to immune-mediated factors, nutritional deficiency states, and disordered myelopoietic responses to various pharmaceutical, herbal, or other potentially myelotoxic compounds. We emphasize the clinical settings, and the histopathologic features, of such AMD that should trigger a search for a reversible underlying condition that may be nonneoplastic and not MDS.

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Čermák, Jaroslav. "Mixed myelodysplastic/myeloproliferative syndromes." Onkologie 10, no. 3 (June 1, 2016): 127–30. http://dx.doi.org/10.36290/xon.2016.027.

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Čermák, Jaroslav. "Myelodysplastic syndromes in 2016." Onkologie 10, no. 3 (June 1, 2016): 114–19. http://dx.doi.org/10.36290/xon.2016.025.

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Kodali, Dhatri, Hector Mesa, Ajay Rawal, Qing Cao, and Pankaj Gupta. "Thrombocytosis in myelodysplastic and myelodysplastic/myeloproliferative syndromes." Leukemia & Lymphoma 48, no. 12 (January 2007): 2375–80. http://dx.doi.org/10.1080/10428190701724827.

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8

Hasserjian, Robert P., Rena Buckstein, and Mrinal M. Patnaik. "Navigating Myelodysplastic and Myelodysplastic/Myeloproliferative Overlap Syndromes." American Society of Clinical Oncology Educational Book, no. 41 (March 2021): 328–50. http://dx.doi.org/10.1200/edbk_320113.

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Myelodysplastic syndromes (MDS) and MDS/myeloproliferative neoplasms (MPNs) are clonal diseases that differ in morphologic diagnostic criteria but share some common disease phenotypes that include cytopenias, propensity to acute myeloid leukemia evolution, and a substantially shortened patient survival. MDS/MPNs share many clinical and molecular features with MDS, including frequent mutations involving epigenetic modifier and/or spliceosome genes. Although the current 2016 World Health Organization classification incorporates some genetic features in its diagnostic criteria for MDS and MDS/MPNs, recent accumulation of data has underscored the importance of the mutation profiles on both disease classification and prognosis. Machine-learning algorithms have identified distinct molecular genetic signatures that help refine prognosis and notable associations of these genetic signatures with morphologic and clinical features. Combined geno-clinical models that incorporate mutation data seem to surpass the current prognostic schemes. Future MDS classification and prognostication schema will be based on the portfolio of genetic aberrations and traditional features, such as blast count and clinical factors. Arriving at these systems will require studies on large patient cohorts that incorporate advanced computational analysis. The current treatment algorithm in MDS is based on patient risk as derived from existing prognostic and disease classes. Luspatercept is newly approved for patients with MDS and ring sideroblasts who are transfusion dependent after erythropoietic-stimulating agent failure. Other agents that address red blood cell transfusion dependence in patients with lower-risk MDS and the failure of hypomethylating agents in higher-risk disease are in advanced testing. Finally, a plethora of novel targeted agents and immune checkpoint inhibitors are being evaluated in combination with a hypomethylating agent backbone to augment the depth and duration of response and, we hope, improve overall survival.

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Matnani, Rahul G., Roshan K. Patel, Stephen E. Strup, and Rouzan G. Karabakhtsian. "5q Minus Myelodysplasia Associated with Multiple Epithelioid Granulomas within Conventional Renal Cell Carcinoma." Case Reports in Pathology 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/138126.

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A 69-year-old Caucasian female, with a previous diagnosis of 5q minus myelodysplastic syndrome, presented with conventional renal cell carcinoma (RCC) associated with multiple-epithelioid nonnecrotizing granulomas. Two previous reports of sarcoidosis, primarily involving the lung and skin, have been described in patients with 5q minus myelodysplasia. A cluster of closely linked genes encoding for cytokines such as IL-4, IL-5, and IL-3 are present on chromosome 5q. Hence, in sarcoidosis, cytokine imbalances associated with the deletion of these cytokine genes have been postulated. However, an occurrence of epithelioid granulomas within a carcinoma, in preexisting clonal myelodysplastic syndrome, has not been described. The patient, in the current study, had long standing 5q minus deletion, clinically characterized by refractory anemia associated with hypolobated megakaryocytes. However, the patient's history was negative for sarcoidosis and the extensive nonnecrotizing epithelioid granulomas were confined within RCC. Due to the absence of Th-2 cytokines, such as IL-4 and IL-5, in a subset of 5q minus myelodysplastic syndrome, proinflammatory Th-1 cytokines such as IFN-γand TNF-αmay be exaggerated in an environment conducive to antigen expression. Hence, we propose a greater susceptibility for the development of granulomas, at least in a subset of patients with 5q minus myelodysplasia.

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Muto, Tomoya, Goro Sashida, Motohiko Oshima, George R. Wendt, Makiko Mochizuki-Kashio, Yasunobu Nagata, Masashi Sanada, et al. "Concurrent loss of Ezh2 and Tet2 cooperates in the pathogenesis of myelodysplastic disorders." Journal of Experimental Medicine 210, no. 12 (November 11, 2013): 2627–39. http://dx.doi.org/10.1084/jem.20131144.

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Polycomb group (PcG) proteins are essential regulators of hematopoietic stem cells. Recent extensive mutation analyses of the myeloid malignancies have revealed that inactivating somatic mutations in PcG genes such as EZH2 and ASXL1 occur frequently in patients with myelodysplastic disorders including myelodysplastic syndromes (MDSs) and MDS/myeloproliferative neoplasm (MPN) overlap disorders (MDS/MPN). In our patient cohort, EZH2 mutations were also found and often coincided with tet methylcytosine dioxygenase 2 (TET2) mutations. Consistent with these findings, deletion of Ezh2 alone was enough to induce MDS/MPN-like diseases in mice. Furthermore, concurrent depletion of Ezh2 and Tet2 established more advanced myelodysplasia and markedly accelerated the development of myelodysplastic disorders including both MDS and MDS/MPN. Comprehensive genome-wide analyses in hematopoietic progenitor cells revealed that upon deletion of Ezh2, key developmental regulator genes were kept transcriptionally repressed, suggesting compensation by Ezh1, whereas a cohort of oncogenic direct and indirect polycomb targets became derepressed. Our findings provide the first evidence of the tumor suppressor function of EZH2 in myeloid malignancies and highlight the cooperative effect of concurrent gene mutations in the pathogenesis of myelodysplastic disorders.

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Dissertations / Theses on the topic "Myelodysplastic"

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Schmidt-Mende, Jan Georg. "Bone marrow apoptosis in myelodysplastic syndromes." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=96939781X.

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Shinde, Sneha. "Role of EZH2 in myelodysplastic syndromes." Thesis, King's College London (University of London), 2015. https://kclpure.kcl.ac.uk/portal/en/theses/role-of-ezh2-in-myelodysplastic-syndromes(323849bf-af95-47e6-8b6d-3393585bfe87).html.

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Occurrence of mutations in the Polycomb (PcG) gene; EZH2 (Enhancer of Zeste Homologue 2) represent a new class of molecular lesions associated with instability in the epigenome of patients with Myelodysplastic Syndrome (MDS). Detection of microdeletion at 7q36.1 or 7q Copy Neutral Loss of Heterozygosity [CN (LOH)] led to the identification of EZH2 mutations. EZH2 is the catalytic component of Polycomb Repressive Complex 2 (PRC2) that trimethylates lysine 27 of histone 3 (H3K27) resulting in gene silencing and recruitment of the sister complex i.e. Polycomb Repressive Complex 1 (PRC1) to target genes. Discovery of EZH2 mutations have shed light on the involvement of other PcG and PcG interacting proteins i.e. Jumonji (jmj) family of demethylases and DNA methyltrasferase 3A (DNMT3A) in MDS. Investigation of Single Nucleotide Polymorphism (SNP) array abnormalities and mutational analysis of these genes have not been ascertained and therefore I examined cytogenetic aberrations affecting twelve Polycomb (PRC1) and seventeen Jumonji genes using high density SNP 6 arrays. SNP6 data analyzed in this study was generated by our group for previous research projects. I visualised this data using CHromosome Analysis Suite (Chas) from Affymetrix and identified five PRC1 genes (BMI1, PHC1, PHC2, RING1A and RING1B) in 17/91 (19 %) patients with either Copy Number Variations (CNVs) like deletions or amplifications or CN (LOH). Interestingly, the frequency of SNP6 aberrations was high (two times) in Jumonji genes as compared to PRC1. 29/91 patients (31 %) showed either CNVs or CN (LOH) in fifteen (JMJD3, JMJD4, JMJD1B, JMJD2A, JARID2, JMJD1C, JARID1B, JMJD2C, UTX, JARID1C, JARID1A, JMJD2D, JHJD1A, JARID1D and JHJD1B) Jumonji genes. Mutational analysis of patients with SNP6 aberrations was carried out using Sanger or 454 sequencing but no mutations were detected in either the PRC1 or Jumonji genes. To elucidate changes in gene expression as a result of amplification or deletion of genomic material, qPCR was performed on 22/29 patients for thirteen Jumonji genes. Gene expression of JARID1A, JARID1C and UTX were modulated concomitant to the CNVs. Deletion of JARID1A locus was associated with reduced gene expression (p value < 0.0001) in two patients while trisomy of JARID1C (n=1) and UTX (n=2) were associated with increased expression (p value < 0.0001) of both the genes. Mutational analysis of PRC2 core components (SUZ12, EED, EZH1) and DNMT3A was carried out in a cohort of 61 MDS patients previously sequenced by our group for EZH2 mutations to examine their mutational overlap. 10/61 patients had heterozygous DNMT3A mutations (clone size 20-44 %) with two patients showing mutations at the R882 site. Interestingly, these mutations were seen predominantly (n= 6) in patients with monosomy 7/del 7q however only one patient had both DNMT3A (R882H) and EZH2 (V626M) mutations suggesting that there is no specific association between mutations of the two genes. In contrast, PRC2 genes were not mutated in this cohort emphasizing the importance of EZH2 mutations alone in MDS pathogenesis. Therefore I examined the functional consequences of the commonly occurring EZH2 (R690C/R690H) and DNMT3A (R882H) mutations in myeloid cell lines. To achieve this, numerous attempts were made to clone DNMT3A R882H mutation into p3XFLAG-myc-CMV-26 to allow transfection and in vitro assessment of the mutant in myeloid cells but all attempts to ligate the plasmid failed and therefore work on DNMT3A was discontinued. EZH2 (R690C/R69H) and Flag tagged wild type EZH2 were constructed in p3XFLAGmyc- CMV-26 vector using a PCR based cloning strategy and transfected into K562 cells. Western blot analysis at 72 hr post transfection, showed elevated levels of both R690C/R690H mutants and Flag tagged wild type EZH2 but no alterations in its target H3K27me3 levels. Affymetrix Human Transcriptome 2.0 gene expression profiling was used to identify modulation of gene signature as result of elevated EZH2 levels and MLLT10 gene was found to be up regulated in cells transfected with Flag-tagged wild type EZH2 (2.3 fold) as well as R690C/ R690H (3.6 – 4.6 fold) mutants. In contrast, PML (promyelocytic leukaemia) (2.16 fold) and FANCL (Fanconi Anaemia, Complementation Group L) (2.18 fold) genes were up regulated exclusively in cells over expressing the Flag tagged wild type EZH2. To compare this gene signature to gene expression changes as a result of EZH2 knock out (KO), shRNA mediated inhibition of EZH2 was carried out in myeloid cells and 95 % KO of both EZH2 and H3K27me3 levels were observed at Day 7 post transduction. Microarray gene expression profiling identified BCL2 (-2.14 fold), FLT1 (-4.03 fold), HOXA10 (-2.2 fold), CD44 (-8.2 fold), CD83 (-2.1 fold), TLSP (-3.24 fold), IFI16 (-3.11 fold) and PAG1 (-3.37 fold) inhibition in cells transduced with shRNA against EZH2 compared to the scrambled and wild type K562 cells. There were no overlapping genes in K562 cells with EZH2 KO and EZH2 mutants R690C/R690H. The differences in expression profiling could be due to the difference in H3K27me3 levels modulated by EZH2. Comparison of gene signature obtained by EZH2 KO on patient samples carrying the R690H mutation, showed contrasting results i.e. up regulation of HOXA10, FLT1, PAG1B, EZH1 and TLSP compared to patients with wild type EZH2 suggesting that EZH2 R690C/R690H mutants do not mimic the transcriptional changes seen in EZH2 KO. This strongly suggests the presence of other mechanisms to compensate for the loss of EZH2 in myeloid cells. However the results obtained here should be examined in additional other myeloid cell lines to validate the findings obtained in K562 cells.

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Abrahamson, Gail Mathilde. "The molecular genetics of the myelodysplastic syndromes." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293790.

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4

梁杏媚 and Hang-mei Polly Leung. "Cellular and molecular aspects of myelodysplastic syndromes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1994. http://hub.hku.hk/bib/B31211628.

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Leung, Hang-mei Polly. "Cellular and molecular aspects of myelodysplastic syndromes /." [Hong Kong : University of Hong Kong], 1994. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13781455.

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Lord, Allegra. "Epigenetics of TET2 Loss in Myelodysplastic Syndromes." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17467483.

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Myelodysplastic syndromes (MDS) are a class of myeloid malignancy characterized by peripheral blood cytopenias and impaired hematopoietic differentiation. Our understanding of the molecular basis of MDS has improved enormously in recent years due to clinical research efforts to characterize the spectrum of acquired mutations found in patients. This work has revealed that mutations in TET2 are common lesions in MDS and other myeloid malignancies. TET2 function has only recently been elucidated: TET proteins convert 5’-methylcytosine (mC) first to 5’-hydroxymethylcytosine (hmC), apparently the first step in an active DNA demethylation program that leads to the replacement of 5-mC with unmodified cytosine. My thesis work focuses on a characterization of TET2 loss on DNA methylation, and on how TET2 mutations impact patient response to treatment with hypomethylating agents. We examined DNA methylation in a matched set of TET2-WT and -mutant MDS samples, and found that loss of TET2 results in global hypermethylation. This global increase is due to gains in intragenic methylation, specifically localized to intron-exon boundaries. We then used clonal TF1 cell lines with CRISPR/Cas9-engineered TET2 mutations to examine global DNA hydroxymethylation. Loss of TET2 results in a global loss of 5-hmC. By aligning our methylation data with hydroxymethylation data from TET2-WT cells, we were able to identify direct TET2 targets. Because changes in mC/hmC with loss of TET2 appeared to localize to intron-exon boundaries, we investigated the effect of aberrant methylation on mRNA splicing in our TF1 cell system. TET2 loss resulted in an overall increase in exon skipping, consistent with published data on the effect of methylation on splicing, and hypermethylated regions were enriched for alternate splicing events. These findings suggest that the alterations in hematopoietic differentiation seen in TET2-mutant models are due to shifts in the expression of different mRNA isoforms rather than wholesale changes in gene expression. Our data show that loss of TET2 function results in region-specific gains in DNA methylation, and that these alterations affect mRNA splicing by promoting exon skipping. Finally, we have found that presence of TET2 mutations are positively associated with response to HMA therapy.
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Williams, Jenna. "The characterisation of telomere dynamics in Myelodysplastic syndromes." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/56965/.

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The Myelodysplastic syndromes (MDSs) are comprised of a heterogeneous group of clonal disorders characterised by ineffective haematopoiesis. Although 30 to 35% of MDS cases progress to Acute Myeloid Leukaemia (AML), the majority of patients die from blood related ailments caused by progressive bone marrow failure. Large-scale genomic rearrangements are a key feature of MDS, with different aberrations conferring specific risks of progression. Telomere erosion, dysfunction and fusion, creating cycles of anaphase bridging breakage and fusion is a mechanism that has the potential to drive genomic instability in many tumour types including MDS. The key aim of this project was to examine the role that telomere dysfunction may play in the generation of genomic rearrangements observed in MDS/AML. High resolution Single Telomere Length Analysis (STELA) revealed telomere shortening when compared to age-matched individuals in two cohorts of MDS and AML patients; this included large-scale telomeric deletion events observed within the MDS cohort. A PCR based telomere fusion assay detected telomere-telomere fusion events at a frequency that was consistent with sporadic fusion arising as a consequence of large-scale deletion. Telomerase activity was up-regulated in AML which may contribute to the reduction of deletion and fusion events in these cells. Sequence analysis revealed that telomere fusion was associated with microhomology and sub-telomeric deletion; this profile was consistent with error-prone Ku-independent alternative end joining processes. Telomere length at diagnosis irrespective of conventional markers appeared to influence the overall survival of MDS patients, but this was not apparent in AML. More importantly, telomere length was able to refine favourable prognostic markers, specifically good risk cytogenetics, uni-lineage cytopenia and low-risk IPSS (International Prognostic Scoring System) scores of which MDS patients bearing shorter telomeres for their respective age displayed reduced overall survival. This may be a particularly important finding given the heterogeneous clinical outcomes observed within low-risk MDS patients.

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Machado, Diogo Alcino de Abreu Ribeiro Carvalho. "Myelodysplastic Syndromes - Therapeutic options in high-risk patients." Dissertação, Instituto de Ciências Biomédicas Abel Salazar, 2009. http://hdl.handle.net/10216/52785.

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Machado, Diogo Alcino de Abreu Ribeiro Carvalho. "Myelodysplastic Syndromes - Therapeutic options in high-risk patients." Master's thesis, Instituto de Ciências Biomédicas Abel Salazar, 2009. http://hdl.handle.net/10216/52785.

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Seal, Sudeshna. "Role of Flice inhibitory protein (FLIP) in myelodysplastic syndromes /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8632.

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Books on the topic "Myelodysplastic"

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Platzbecker, Uwe, and Pierre Fenaux, eds. Myelodysplastic Syndromes. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-76879-3.

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Deeg, H. Joachim, David T. Bowen, Steven D. Gore, Torsten Haferlach, Michelle M. Le Beau, and Charlotte Niemeyer. Myelodysplastic Syndromes. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36229-3.

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Schmalzl, Franz, and G. J. Mufti, eds. Myelodysplastic Syndromes. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-75952-9.

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Várkonyi, Judit. The Myelodysplastic Syndromes. Dordrecht: Springer Science+Business Media B.V., 2011.

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Várkonyi, Judit, ed. The Myelodysplastic Syndromes. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0440-4.

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Deeg, H. J., D. T. Bowen, S. D. Gore, T. Haferlach, M. M. Le Beau, and C. Niemeyer. Hematologic Malignancies: Myelodysplastic Syndromes. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-30794-x.

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List, Alan. Clinician’s Manual on Myelodysplastic Syndromes. Tarporley: Springer Healthcare Ltd., 2008.

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List, Alan. Clinician’s Manual on Myelodysplastic Syndromes. Tarporley: Springer Healthcare Ltd., 2008. http://dx.doi.org/10.1007/978-1-907673-36-8.

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Nazha, Aziz, ed. Diagnosis and Management of Myelodysplastic Syndromes. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51878-3.

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Lenn, Fechter, ed. 100 questions & answers about myelodysplastic syndromes. Sudbury, Mass: Jones and Bartlett Publishers, 2008.

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Book chapters on the topic "Myelodysplastic"

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Bennett, J. M. "The Classification of Myelodysplastic Syndromes." In Myelodysplastic Syndromes, 3–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-75952-9_1.

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Koeller, U., O. Krieger, O. A. Haas, P. Bettelheim, O. Majdic, and W. Knapp. "Immunological Phenotyping of Blood and Bone Marrow Cells From Patients with Myelodysplastic Syndromes." In Myelodysplastic Syndromes, 60–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-75952-9_10.

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Lambertenghi-Deliliers, G., D. Soligo, C. Annaloro, E. Pozzoli, and A. Riva. "Bone Marrow Biopsy in RAEB and RAEB-t Myelodysplastic Syndromes." In Myelodysplastic Syndromes, 67–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-75952-9_11.

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Quaglino, D., and F. Schmalzl. "Discussion of Poster Session I." In Myelodysplastic Syndromes, 74–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-75952-9_12.

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Dörmer, P. "Maturation Pattern and Evolution of Leukemia in the Myelodysplastic Syndrome." In Myelodysplastic Syndromes, 81–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-75952-9_13.

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Brunning, R. D. "Therapy-Related Myelodysplastic Syndromes and Acute Myeloid Leukemia." In Myelodysplastic Syndromes, 90–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-75952-9_14.

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Tricot, G. J., M. T. Rizzo, and C. De Wolf-Peeters. "The Prognostic Value of Abnormal Localization of Immature Precursors in the Myelodysplastic Syndromes." In Myelodysplastic Syndromes, 99–102. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-75952-9_15.

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Frisch, B., and R. Bartl. "Bone Marrow Histology in Myelodysplastic Syndromes: An Update." In Myelodysplastic Syndromes, 103–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-75952-9_16.

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Bartl, R., B. Frisch, and C. Schmid. "Evolution of Myelodysplastic Syndromes." In Myelodysplastic Syndromes, 107–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-75952-9_17.

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Schmid, C., R. Bartl, K. Jäger, A. Beham, H. Seewann, G. Kettner, and B. Frisch. "Conversion of Myelodysplastic Subtypes to Acute Leukemia: A Follow-Up Study." In Myelodysplastic Syndromes, 114–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-75952-9_18.

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Conference papers on the topic "Myelodysplastic"

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Sidek, Norsima Nazirah, M. Y. Mashor, and R. Hassan. "Review article a perspective of Myelodysplastic Syndrome (MDS)." In 2012 International Conference on Biomedical Engineering (ICoBE). IEEE, 2012. http://dx.doi.org/10.1109/icobe.2012.6179072.

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Kadri, M., R. Patel, A. Al-khateeb, M. Hussain, S. Bellary, H. Sharma, R. A. Miller, and K. Alan. "Sarcomatoid Mesothelioma in a Patient with Myelodysplastic Syndrome." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6954.

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Yoshida, Kenichi, Masashi Sanada, Yasunobu Nagata, Ryoichiro Kawahata, Motohiro Kato, Aiko Matsubara, Jyunko Takita, et al. "Abstract 925: Whole exome analysis of myelodysplastic syndromes." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-925.

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4

Beck, Dominik, Miriam Brandl, Tuan D. Pham, Chung-Che Chang, Xiaobo Zhou, Tuan D. Pham, Xiaobo Zhou, et al. "In-Silico Identification Of Micro-Loops In Myelodysplastic Syndromes." In 2011 INTERNATIONAL SYMPOSIUM ON COMPUTATIONAL MODELS FOR LIFE SCIENCES (CMLS-11). AIP, 2011. http://dx.doi.org/10.1063/1.3596650.

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5

Ebert, Benjamin. "Abstract SY13-03: Novel targeted therapies in myelodysplastic syndrome." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-sy13-03.

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6

Aanei, Carmen-Mariana, Pascale Flandrin-Gresta, Françoise Solly, Florin Zugun-Eloae, Eugen Carasevici, Emmanuelle Tavernier, Denis Guyotat, and Lydia Campos-Guyotat. "Abstract 2470: Adhesion-mediated dysfunctions in myelodysplastic syndromes microenvironment." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2470.

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BELISARIO, THAIS CHAVES, KETTY LYSIE LIBARDI LIRA MACHADO, LUIZA CORRÊA RODRIGUES, ISABELLA RABELO FARIA, MARIA CARMEN LOPES FERREIRA SILVA SANTOS, LETÍCIA FONSECA FAVARATO, WEIDER ANDRADE TOMÉ, et al. "A RARE ASSOCIATION BETWEEN MYELODYSPLASTIC SYNDROME AND IGA VASCULITIS." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-014.

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Zhang, Xuefang, Libo Jiang, Shuying Zhang, Heng Guo, and Hong Zhou. "Expression and Significance of CD123 and CD96 in Myelodysplastic Syndrome." In International Conference on Electronics, Mechanics, Culture and Medicine. Paris, France: Atlantis Press, 2016. http://dx.doi.org/10.2991/emcm-15.2016.124.

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9

Al-Bakhat, Lama, and Norah Al-Serhani. "LncRNAs and Protein-coding Genes Expression Analysis for Myelodysplastic Syndromes Diagnoses." In 2020 International Conference on Artificial Intelligence & Modern Assistive Technology (ICAIMAT). IEEE, 2020. http://dx.doi.org/10.1109/icaimat51101.2020.9308011.

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Nazha, Aziz, David Seastone, Hideki Makishima, Matt Kalaycio, Hetty E. Carraway, Anjali S. Advani, Ahamd Zarzour, et al. "Abstract 5575: Obesity and genomic changes in patients with myelodysplastic syndromes." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5575.

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Reports on the topic "Myelodysplastic"

1

Starczynowski, Daniel. Regulation and Function of TIFAB in Myelodysplastic Syndrome. Fort Belvoir, VA: Defense Technical Information Center, August 2014. http://dx.doi.org/10.21236/ada613223.

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2

Starczynowski, Daniel. Regulation and Function of TIFAB in Myelodysplastic Syndrome. Fort Belvoir, VA: Defense Technical Information Center, June 2012. http://dx.doi.org/10.21236/ada567467.

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3

Starczynowski, Daniel. Regulation and Function of TIFAB in Myelodysplastic Syndrome. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada585851.

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4

Lindner, Daniel. Complementation of Myelodysplastic Syndrome Clones with Lentivirus Expression Libraries. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada566912.

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Lindner, Daniel. Complementation of Myelodysplastic Syndrome Clones with Lentivirus Expression Libraries. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada581646.

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6

Lindner, Daniel J. Complementation of Myelodysplastic Syndrome Clones with Lentivirus Expression Libraries. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada581503.

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7

Walter, Matthew J. The Role of U2AF1 Mutations in the Pathogenesis of Myelodysplastic Syndromes. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613973.

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8

Park, Christopher Y. Functional Role of MicroRNAs in Hematopoietic Stem Cells in the Myelodysplastic Syndromes. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada575806.

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