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Journal articles on the topic 'Myelodysplastic'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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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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2

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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3

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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4

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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5

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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6

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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7

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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9

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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10

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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11

Singh, M., A. Bofinger, R. Ba Pe, and K. Taylor. "Myelodysplasia with myelofibrosis — A distinct subgroup within the myelodysplastic syndromes." Pathology 26, no. 1 (1994): 69–71. http://dx.doi.org/10.1080/00313029400169171.

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12

Geissler, R. Georg, and Arnold Ganser. "Myelodysplastic Syndromes." BioDrugs 10, no. 2 (1998): 97–109. http://dx.doi.org/10.2165/00063030-199810020-00002.

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13

Cheong, June Won, and Yoo Hong Min. "Myelodysplastic Syndrome." Journal of the Korean Medical Association 49, no. 10 (2006): 897. http://dx.doi.org/10.5124/jkma.2006.49.10.897.

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14

_, _. "Myelodysplastic Syndromes." Journal of the National Comprehensive Cancer Network 6, no. 9 (October 2008): 902. http://dx.doi.org/10.6004/jnccn.2008.0069.

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Myelodysplastic syndromes (MDS) represent myeloid clonal hemopathies with relatively heterogeneous spectrums of presentation. The major clinical problems in these disorders are morbidities caused by patients' cytopenias and the potential for MDS to evolve into acute myeloid leukemia (AML). Managing MDS is complicated by the generally advanced age of patients, attendant non-hematologic comorbidities, and older patients' relative inability to tolerate some therapies. In addition, when the illness progresses into AML, these patients experience lower response rates to standard therapy than patients with de novo AML. Important changes from the 2008 version of the guidelines include the addition of lenalidomide as a possible treatment for symptomatically anemic non-del(5q) patients whose anemia does not respond to initial therapy. For the most recent version of the guidelines, please visit NCCN.org
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15

Greenberg, Peter L., Eyal Attar, John M. Bennett, Clara D. Bloomfield, Carlos M. De Castro, H. Joachim Deeg, James M. Foran, et al. "Myelodysplastic Syndromes." Journal of the National Comprehensive Cancer Network 9, no. 1 (January 2011): 30–56. http://dx.doi.org/10.6004/jnccn.2011.0005.

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16

Greenberg, Peter L., Eyal Attar, John M. Bennett, Clara D. Bloomfield, Uma Borate, Carlos M. De Castro, H. Joachim Deeg, et al. "Myelodysplastic Syndromes." Journal of the National Comprehensive Cancer Network 11, no. 7 (July 2013): 838–74. http://dx.doi.org/10.6004/jnccn.2013.0104.

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17

Neumeister, Peter, Richard Pestell, Beate Balent, Gerald Jaeger, Werner Linkesch, and Heinz Sill. "Myelodysplastic Syndrome." American Journal of Cancer 1, no. 5 (2002): 301–11. http://dx.doi.org/10.2165/00024669-200201050-00001.

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18

Nakao, Shinji, H. Joachim Deeg, Takayuki Ishikawa, Judith Marsh, Alan List, and Masao Tomonaga. "Myelodysplastic Syndrome." International Journal of Hematology 82, no. 5 (December 1, 2005): 412–16. http://dx.doi.org/10.1532/ijh97.05139.

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19

Killick, Sally B. "Myelodysplastic disorders." Medicine 37, no. 4 (April 2009): 186–89. http://dx.doi.org/10.1016/j.mpmed.2008.12.003.

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20

Killick, Sally B. "Myelodysplastic disorders." Medicine 41, no. 5 (May 2013): 261–64. http://dx.doi.org/10.1016/j.mpmed.2013.03.007.

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21

Carvalhosa, Ana, and Sally B. Killick. "Myelodysplastic disorders." Medicine 45, no. 5 (May 2017): 270–74. http://dx.doi.org/10.1016/j.mpmed.2017.02.006.

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22

Steensma, David P. "Myelodysplastic Syndromes." Hematology/Oncology Clinics of North America 34, no. 2 (April 2020): xv—xvi. http://dx.doi.org/10.1016/j.hoc.2019.12.001.

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23

Adès, Lionel, Raphael Itzykson, and Pierre Fenaux. "Myelodysplastic syndromes." Lancet 383, no. 9936 (June 2014): 2239–52. http://dx.doi.org/10.1016/s0140-6736(13)61901-7.

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24

Cachia, P. G., and R. A. Padua. "Myelodysplastic Syndromes." Scottish Medical Journal 39, no. 1 (February 1994): 5–7. http://dx.doi.org/10.1177/003693309403900102.

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25

Orazi, Attilio, and Magdalena B. Czader. "Myelodysplastic Syndromes." American Journal of Clinical Pathology 132, no. 2 (August 2009): 290–305. http://dx.doi.org/10.1309/ajcprcxx4r0yhkwv.

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26

Ungerstedt, Johanna. "Myelodysplastic syndromes." HemaSphere 3 (June 2019): 131. http://dx.doi.org/10.1097/hs9.0000000000000253.

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27

Bick, Rodger L., and W. Robert Laughlin. "Myelodysplastic Syndromes." Laboratory Medicine 24, no. 11 (November 1, 1993): 712–16. http://dx.doi.org/10.1093/labmed/24.11.712.

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28

Scott, Bart L., and H. Joachim Deeg. "Myelodysplastic Syndromes." Annual Review of Medicine 61, no. 1 (February 2010): 345–58. http://dx.doi.org/10.1146/annurev.med.051308.132852.

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29

Hofmann, Wolf-K., and H. Phillip Koeffler. "Myelodysplastic Syndrome." Annual Review of Medicine 56, no. 1 (February 2005): 1–16. http://dx.doi.org/10.1146/annurev.med.56.082103.104704.

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30

Dao, Kim-Hien T. "Myelodysplastic Syndromes." Medical Clinics of North America 101, no. 2 (March 2017): 333–50. http://dx.doi.org/10.1016/j.mcna.2016.09.006.

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31

Yeomans, Anita C., and Margaret T. Harle. "Myelodysplastic syndromes." Seminars in Oncology Nursing 6, no. 1 (February 1990): 9–16. http://dx.doi.org/10.1016/s0749-2081(05)80128-7.

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32

Utley, Susan M. "Myelodysplastic syndromes." Seminars in Oncology Nursing 12, no. 1 (February 1996): 51–58. http://dx.doi.org/10.1016/s0749-2081(96)80018-0.

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33

Steensma, David P. "Myelodysplastic Syndromes." Mayo Clinic Proceedings 90, no. 7 (July 2015): 969–83. http://dx.doi.org/10.1016/j.mayocp.2015.04.001.

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34

Steensma, David P. "Myelodysplastic Syndromes." Hematology/Oncology Clinics of North America 34, no. 2 (April 2020): i. http://dx.doi.org/10.1016/s0889-8588(20)30003-4.

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35

Nimer, Stephen D. "Myelodysplastic syndromes." Blood 111, no. 10 (May 15, 2008): 4841–51. http://dx.doi.org/10.1182/blood-2007-08-078139.

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Abstract There has been a remarkable explosion of knowledge into the molecular defects that underlie the acute and chronic leukemias, leading to the introduction of targeted therapies that can block key cellular events essential for the viability of the leukemic cell. Our understanding of the pathogenesis of the myelodysplastic syndromes (MDSs) has lagged behind, at least in part, because they represent a more heterogeneous group of disorders. The significant immunologic abnormalities described in this disease, coupled with the admixture of MDS stem or progenitor cells within the myriad types of dysplastic and normal cells in the bone marrow and peripheral blood, have made it difficult to molecularly characterize and model MDS. The recent availability of several, effective (ie, FDA-approved) therapies for MDS and newly described mouse models that mimic aspects of the human disease provide an opportune moment to try to leverage this new knowledge into a better understanding of and better therapies for MDS.
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36

Maslak, P. "Myelodysplastic syndrome." ASH Image Bank 2002, no. 0719 (July 19, 2002): 100391. http://dx.doi.org/10.1182/ashimagebank-2002-100391.

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37

Legare, Robert D., and Gary D. Gilliland. "Myelodysplastic syndrome." Current Opinion in Hematology 2, no. 4 (1995): 283–92. http://dx.doi.org/10.1097/00062752-199502040-00008.

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38

Forman, Stephen J. "Myelodysplastic syndrome." Current Opinion in Hematology 3, no. 4 (1996): 297–302. http://dx.doi.org/10.1097/00062752-199603040-00008.

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39

Ma, Xiaomei, Monique Does, Azra Raza, and Susan T. Mayne. "Myelodysplastic syndromes." Cancer 109, no. 8 (April 15, 2007): 1536–42. http://dx.doi.org/10.1002/cncr.22570.

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40

Van Dang, Chi. "Myelodysplastic Syndrome." JAMA: The Journal of the American Medical Association 267, no. 15 (April 15, 1992): 2077. http://dx.doi.org/10.1001/jama.1992.03480150083042.

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41

Dang, C. V. "Myelodysplastic syndrome." JAMA: The Journal of the American Medical Association 267, no. 15 (April 15, 1992): 2077–80. http://dx.doi.org/10.1001/jama.267.15.2077.

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42

TAKAKU, Fumimaro. "Myelodysplastic syndrome." Nihon Naika Gakkai Zasshi 74, no. 9 (1985): 1223–26. http://dx.doi.org/10.2169/naika.74.1223.

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43

YOSHIDA, YATARO. "Myelodysplastic syndrome." Nihon Naika Gakkai Zasshi 82, no. 9 (1993): 1566–70. http://dx.doi.org/10.2169/naika.82.1566.

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44

Hofmann, Wolf-Karsten, Michael Lübbert, Dieter Hoelzer, and H. Phillip Koeffler. "Myelodysplastic syndromes." Hematology Journal 5, no. 1 (2004): 1–8. http://dx.doi.org/10.1038/sj.thj.6200335.

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45

Maslak, P. "Myelodysplastic syndrome." ASH Image Bank 2002, no. 0918 (September 18, 2002): 100458. http://dx.doi.org/10.1182/ashimagebank-2002-100458.

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46

Maslak, P. "Myelodysplastic syndrome." ASH Image Bank 2002, no. 0923 (September 23, 2002): 100467. http://dx.doi.org/10.1182/ashimagebank-2002-100467.

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47

Schrier, S. "Myelodysplastic Syndrome." ASH Image Bank 2002, no. 1016 (October 16, 2002): 100508. http://dx.doi.org/10.1182/ashimagebank-2002-100508.

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48

Wells, Richard A., Rena Buckstein, and Jeremy Rezmovitz. "Myelodysplastic syndrome." Canadian Medical Association Journal 188, no. 10 (January 4, 2016): 751. http://dx.doi.org/10.1503/cmaj.151077.

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49

Yeomans, Anita C. "Myelodysplastic syndromes." Cancer Nursing 10, no. 1 (February 1987): 32???40. http://dx.doi.org/10.1097/00002820-198702000-00005.

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50

Hann, I. M. "Myelodysplastic syndromes." Archives of Disease in Childhood 67, no. 7 (July 1, 1992): 962–66. http://dx.doi.org/10.1136/adc.67.7.962.

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