2 research outputs found

    A chronic myelomonocytic leukemia (CMML)–like myelodysplastic/myeloproliferative disorder in -deficient mice

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    ) Complete blood counts (white blood cell, lymphocyte, neutrophil, monocyte, red blood cell [RBC], hemoglobin, platelet) in wild-type mice at 2–5 months of age (n = 35), in mice at 2–5 months of age (n = 30), in wild-type mice more than 5 months old (n = 25), and in mice more than 5 months old with symptoms of CMML (n = 25). Means (and 95% confidence intervals) for cell concentrations are shown, and values were calculated using Student test. ) Wright–Giemsa staining of peripheral blood from an mouse with symptoms of CMML, showing teardrop poikilocytes (a, ), red cells with Howell–Jolly bodies (b, ), and nucleated red cells (c, ). Immature (d, ) and maturing (d, ) mononuclear cells were also observed, together with phagocytosis of RBC by a monocyte (e, ). Ten separate analyses were performed. = 5 μm. ) Survival of (n = 25) mice and wild-type (n = 25) mice. ) Reticulin staining of paraffin sections of bone marrow from a wild-type mouse and a sick mouse. The sample shows fibrous tissue stained with black color. Scale bars = 20 μm. ) Flow cytometric analysis of apoptotic cells in bone marrow from a wild-type and a sick mouse. The percentages of cells positive for annexin V are indicated. Five separate cytometric analyses were performed. ) Splenomegaly and ) hepatomegaly in a sick mouse. Hematoxylin and eosin–stained sections of ) spleen and ) liver from a wild-type mouse and a sick mouse. Extramedullary hematopoiesis was found in the spleen and liver, which were infiltrated with nucleated elements of blood cells. Ten separate analyses were performed. Scale bars = 20 μm. ) Flow cytometric analysis of cells from spleen in a wild-type mouse and an mouse stained with Ter119 surface antigen. The percentages of cells positive for the antigen are indicated. Twenty separate analyses were performed.<p><b>Copyright information:</b></p><p>Taken from "Identification of Chromatin Remodeling Genes and as Leukemia Suppressor Genes"</p><p></p><p>JNCI Journal of the National Cancer Institute 2008;100(17):1247-1259.</p><p>Published online 3 Sep 2008</p><p>PMCID:PMC2528019.</p><p></p

    Gene expression analysis of bone marrow cells from wild-type, , and mice

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    ) Reverse transcriptase–polymerase chain reaction was performed to analyze the genes indicated, with serving as the control gene. Three separate experiments were performed. ) Pathways by which and might regulate hematopoiesis through control of the and genes. In the scenario shown, controls erythropoiesis, possibly by positively regulating and genes. also controls the expression of , whose product blocks differentiation of hematopoietic stem cells and common myeloid progenitors. Control of B lymphopoiesis by may be achieved by increasing expression of . , together with , increases expression of , which acts on regulatory T (TR) cells to suppress conventional T (Tc) cells. also functions as a tumor suppressor gene. However, it is unclear whether suppresses leukemia malignancies.<p><b>Copyright information:</b></p><p>Taken from "Identification of Chromatin Remodeling Genes and as Leukemia Suppressor Genes"</p><p></p><p>JNCI Journal of the National Cancer Institute 2008;100(17):1247-1259.</p><p>Published online 3 Sep 2008</p><p>PMCID:PMC2528019.</p><p></p
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