Linked Life Data

21421110

Source:http://linkedlifedata.com/resource/pubmed/id/21421110

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pubmed-article:21421110pubmed:abstractTextMyeloid neoplasms are characterized by acquired somatic mutations and epigenetic alterations in genes that are crucial for hematopoietic differentiation and cellular proliferation and survival pathways. The heterogeneity and genetic complexity of these disorders is daunting, but the improvement in our knowledge of the pathogenetic mechanisms underlying myeloid transformation, coupled with the increasing availability of agents that target these pathways, offers unique opportunities for improved therapy. This review will focus on common mutations that are of therapeutic or prognostic importance in acute myeloid leukemia (AML) and the classic Philadelphia chromosome-negative myeloproliferative neoplasms (Ph(-) MPNs), in the context of discussing the potential for risk-adapted and targeted therapeutic approaches for these diseases.lld:pubmed
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pubmed-article:21421110pubmed:copyrightInfoCopyright © 2011 Elsevier Inc. All rights reserved.lld:pubmed
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pubmed-article:21421110pubmed:volume38lld:pubmed
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pubmed-article:21421110pubmed:year2011lld:pubmed
pubmed-article:21421110pubmed:articleTitleGene mutations, epigenetic dysregulation, and personalized therapy in myeloid neoplasia: are we there yet?lld:pubmed
pubmed-article:21421110pubmed:affiliationDepartment of Medicine, The University of Chicago, Chicago, IL 60637, USA. todenike@medicine.bsd.uchicago.edulld:pubmed
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