Author Archives: azaleaazelia

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CHRONIC LYMPHOCYTIC LEUKEMIA part 29

  Finally, transfer of human B-CLL cells into immune-deficient mice may bypass the ex vivo apoptosis tendency of B-CLL cells, enabling their survival and amplification in vivo. Such an approach may also make it possible to define and test new … Continue reading

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CHRONIC LYMPHOCYTIC LEUKEMIA part 28

  In the third tramsgenic model, overexpression of APRIL (a proliferation inducing ligand ) in murine T cells leads indirectly¬† to B-cell proliferation and survival because of signaling through its receptors BCMA and TACI. Unlike the previous two transgenic animals, … Continue reading

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CHRONIC LYMPHOCYTIC LEUKEMIA part 27

  Another mouse model that develops features resembling human B-CLL involves the overexpression of two genes: BCL-2 and TRAFT2 (TNF-receptor-associated factor 2). This double transgenic animal is especially intriguing because of the already mentioned recent work showing¬† that the deletion … Continue reading

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CHRONIC LYMPHOCYTIC LEUKEMIA part 26

  Transgenic mice expressing the TCL1 gene in murine B cells develop a polyclonal expression of B lymphocytes early in life that becomes progressively more restricted until a monoclonal population emerges after about one year in most animals. The genetic … Continue reading

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CHRONIC LYMPHOCYTIC LEUKEMIA part 25

  In recent years, however,¬† a variety of transgenic mouse models have been developed that lead to diseased phenotypes resembling human B-CLL more closely and reproducibly. We focus on three models that have been especially helpful.

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CHRONIC LYMPHOCYTIC LEUKEMIA part 24

  ANIMAL MODELS OF B-CLL While an enormous amount of new information has been gleaned by directly studying human B-CLL cells, animal models are now contributing to our understanding of the human disease. For example, New Zealand Black (NZB) mice … Continue reading

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CHRONIC LYMPHOCYTIC LEUKEMIA part 23

  Because in vitro observations demonstrate the absence of lesions in the major apoptotic pathways, the model posits the absence of an intrinsic cell death defect in the majority of the leukemic clones. We do not rule out the possibility … Continue reading

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