Abstract
In this work different types of dysregulation of signaling proteins in the context of myeloproliferative neoplasms are examined. In this heterogeneous disease group, uncontrolled cell proliferation plays acrucial role for the initiation of tumorigenesis, which Robert Weinberg described as a"hallmark" for the development of cancer. Protein dysregulation in form of overexpression of GAB2, aprotein involved in formation of the CML-pathognomonic BCR/ABL-translocation complex, results in an enhanced disease phenotype in aBcr/Abl-positive mouse model and disease acceleration is associated with achange of the subcellular localization of GAB2 in human blasts in CML-bone marrow biopsies. Furthermore, analyses of amouse model show that aprotein dysregulation caused by adistinct translocation (Tel-Syk) leads to the formation of aspecific and morphologically very characteristic phenotype in the bone marrow of diseased mice. Moreover, results were presented which show that in certain subgroups of Myeloproliferative Neoplasms the protein NFE2, which is initially known only as atranslocating factor, is apparently regulated by altering its subcellular localization. The difference in the subcellular localization of NFE2 in erythroid bone marrow cells is so clear between Essential Thrombocythemia and Primary Myelofibrosis that quantitative NFE2 immunohistochemistry can be used as an ancillary tool to diagnostically discriminate these two entities in an early stage.
Published Version
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