• Journal of Yeungnam Medical Science
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• v.8 no.2
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• pp.209-216
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• 1991

Acute Megakaryoblastic leukemia is a rare and rapidly fatal disease characterized by proliferation of megakaryocyte series and atypical megakaryocytes in the bone marrow. Acute Megakaryoblastic leukemia is suspicious when 1) megakaryocyte in peripheral blood, mixture of large and small mononuclear megakaryoblast in the bone marrow 2) cytoplasmic budding in blast 3) myelofibrosis (dense medullary overgrowth of reticulin fibers) 4) PAS(+), ANAE(+), SBB(-), peroxidase(-) and which is confirmed by platelet peroxidase oxidation on electromicroscope or monoclonal antibody. A case of aute megakaryoblastic leukemia was studied morphologically and monoclonal antibody.

• BMB Reports
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• v.47 no.6
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• pp.299-310
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• 2014

Cohesin is a multi-protein complex composed of four core subunits (SMC1A, SMC3, RAD21, and either STAG1 or STAG2) that is responsible for the cohesion of sister chromatids following DNA replication until its cleavage during mitosis thereby enabling faithful segregation of sister chromatids into two daughter cells. Recent cancer genomics analyses have discovered a high frequency of somatic mutations in the genes encoding the core cohesin subunits as well as cohesin regulatory factors (e.g. NIPBL, PDS5B, ESPL1) in a select subset of human tumors including glioblastoma, Ewing sarcoma, urothelial carcinoma, acute myeloid leukemia, and acute megakaryoblastic leukemia. Herein we review these studies including discussion of the functional significance of cohesin inactivation in tumorigenesis and potential therapeutic mechanisms to selectively target cancers harboring cohesin mutations.